Hemostasis I Flashcards

1
Q

Hemostasis components

A
  • vascular system
  • platelet system
  • coagulation system
  • fibrinolytic system
  • coagulation inhibition system
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2
Q

Mechanism of hemostasis

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

Causes of vascular constriction in hemostasis

A
  1. Platelet-released thromboxane A2

2. nervous system reflex to pain

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4
Q

Formation of platelet plug (primary hemostasis)

A

Injury–> Collagen + VWF + PLTs + fibrinogen

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5
Q

How are platelets activated

A
  1. Binding of VWF to GPIb

2. Thrombin, adrenalin, ADP, collagen

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6
Q

Activated platelets release?

A

ADP, thromboxane, Calcium

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7
Q

Activation of plts by ADP exposes what receptor?

A

GPIIb/IIIa

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8
Q

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

A

thromboxane A2

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9
Q

Function of GPIIb/IIIa

A

Receptor that binds to fibrinogen, linking platelets together

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10
Q

Secondary hemostasis

A

Clot formation

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11
Q

Function of thrombin in hemostasis?

A

Fibrin conversion, platelet activation

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12
Q

Name for Factor I

A

Fibrinogen

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13
Q

Name for Factor 2

A

Prothrombin

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14
Q

Name for Factor 3

A

Tissue factor or thromboplastin

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15
Q

Name for Factor 4

A

Calcium

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16
Q

Name for factor 13

A

Fibrin-stabilizing factor

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17
Q

Prothrombin is converted to thrombin by the action of what?

A

Prothrombin activator

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18
Q

fibrinogen is converted to fibrin monomer and eventually fibrin fibers by

A

Thrombin

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19
Q

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

A

Factor 13. Fibrin-stabilizing factor

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20
Q

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

A

COXs pathways to inhibit the production of thromboxane A2

21
Q

Extrinsic pathway is activated by?

A

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

22
Q

Primary factor in the extrinsic pathway

A

Factor 7

23
Q

TF:FVII activates what factor?

A

Factor ten, and is considered a TENase

24
Q

Intrinsic pathway is activated by?

A

Trauma to the blood, or exposure to collagen

25
Q

Factors specific to the intrinsic pathway

A

12, 11, 9, 8

26
Q

Factors of the common pathway

A

10, 5, 2, 1

27
Q

Final common pathway

A

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

28
Q

In the contemporary view of hemostasis coagulation begins with the activation of factors X and IX by?

A

TF:FVII complex, thus, linking the intrinsic and extrinsic pathway

29
Q

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

A
  1. Initial phase
  2. Amplification phase
  3. Propagation phase
30
Q

Initiation phase

A

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

31
Q

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

A

small

32
Q

Amplification phase

A

-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
Q

Factors thrombin acts on in the positive feedback loop

A

11–>11a, 8–>8a, 5–>5a

**Thrombin also leads to further PLT activation and aggregation

34
Q

Propagation phase

A

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
Q

Fibrinolysis

A

Dissolution of thrombi and maintaining patency of vascular system

36
Q

Fibrinolysis pathway

A

Plasminogen activated to plasmin which cleaves fibrin

37
Q

Factors that activate plasminogen

A

Physiologic- tPA, Urokinase

Exogenous- Streptokinase

38
Q

Medications that block plasmin from cleaving thrombin

A

Amicar

Tranexamic acid

39
Q

Hemophilia A is a deficiency in what factor?

A

Factor VIII

40
Q

Severe hemophilia

A

<1% of normal factors

41
Q

Mild hemophilia

A

> 5% but <40% normal factors

42
Q

Hemophilia B

A

Factor IX deficiency

43
Q

Treatment for hemophilia

A
  • Replacement of factor
  • DDAVP
  • sometimes antifibrinolytics
44
Q

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

A

antifactor antibodies

45
Q

Disseminated intravascular coagulation

A

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

46
Q

Common conditions that cause DIC

A

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

47
Q

Management of DIC primarily focuses on treating?

A

the underlying disorder

48
Q

DIC diagnosis

A

plts 10-20k

  • Symptoms of thrombosis
  • Bleeding from three unrelated sites
  • Lab findings- prolonged clotting times, decreased clotting factors