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MOD > Hemodynamic Disorders (4) - Hemostasis, section 2 > Flashcards

Hemodynamic Disorders (4) - Hemostasis, section 2 Flashcards

1
Q

Hemostasis

A

Formation of a blood clot to stop blood flow

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2
Q

What are the 4 steps to Hemostasis

A
  1. Arterial Vasoconstriction
  2. Primary Hemostasis - platelet plug
  3. Secondary Hemostasis - fibrin deposition
  4. Clot stabilization and resorption
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3
Q

What causes vasoconstriction?

A

Endothelin

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4
Q

What are the 3 steps of platelets during primary hemostasis?

A
  1. Adhesion
  2. Activation
  3. Aggregation
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5
Q

What molecule on the subendeothelial surface is involved with platelet adhesion?

A

Von Willebrand Factor (vWF)

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6
Q

What molecule on the platelet surface is involved with platelet adhesion?

A

GP1b

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7
Q

What binds to what for platelet adhesion during primary hemostasis?

A

GP1b binds to Von Willebrand Factor

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8
Q

What molecule activates platelets during primary hemostasis?

A

Thrombin

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9
Q

Platelet activation involves 3 structural changes. Describe those.

A
  1. Conformational change of the platelet (increased surface area) and GP2b-3a (concave)
  2. Negatively charged platelet surface
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10
Q

Platelet activation involves release of 2 types of granules. What are those?

A

Dense granules

Alpha granules

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11
Q

Platelet activation causes release of granules from the platelet. What molecule release causes more platelet activation?

A

ADP

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12
Q

Platelet activation causes release of granules from the platelet. What molecule release causes platelet aggregation?

A

Thromboxane A2

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13
Q

What does Aspirin inhibit?

A

Thromboxane A2 - Platelet aggregation during primary hemostasis

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14
Q

For platelet aggregation, what receptor on the platelet is involved?

A

GP2b-3a

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15
Q

For platelet aggregation, what binds to GP2b-3a?

A

Fibrinogen

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16
Q

Fibrinogen binding to GP2b-3a allows for?

A

Cross linking of platelets and forms platelet plug

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17
Q

What is contained in endothelial cells and is a source of von willebrand factor?

A

Weibel Palade Bodies

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18
Q

Where does von willebrand factor come from?

A

Weibel Palade Bodies in the endothelial cells

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19
Q

Von willebrand factor disease

A

Lack of von willebrand factor

- Trouble with platelet adhesion

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20
Q

Bernard Soulier Syndrome

A

Lack of GP1b

- Trouble with platelet adhesion

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21
Q

How do platelets appear with Bernard Soulier Syndrome?

A

GIANT

22
Q

Glanzmann Thrombasthenia

A

Lack of GP2b-3a

- Trouble with platelet aggregation

23
Q

Thrombocytopenia

A

LOW platelets (less than 50K)

24
Q

What occurs during secondary hemostasis?

A

Fibrin deposition and coagulation cascade

= clot stabilization

25
Q

Describe the Intrinsic pathway of secondary hemostasis

A

Factor XII
Factor XI
Factor IX + Factor VIII
- Common pathway

26
Q

Describe the Extrinsic pathway of secondary hemostasis

A

Tissue factor + Factor VII

- Common pathway

27
Q

Describe the Common pathway of secondary hemostasis

A 
Factors IX, VIII, VII activate Factors X and V
Factor II (thrombin)
Fibrinogen activated to Fibrin = stable clot
28
Q

What measures the Extrinsic pathway

A

PT (prothrombin time)

29
Q

What measures the Intrinsic pathway

A

aPTT

30
Q

PT test

A

Tissue factor + blood

- A clot should form in less than 14 seconds

31
Q

aPTT test

A

Negative surface calcium + blood

- A clot should form in less than 45 seconds

32
Q

Anti - Hemophilic A factor

A

Factor VIII

33
Q

Vitamin K dependent factors require?

A

Calcium

34
Q

What are the Vitamin K dependent factors?

A

2, 7, 9, 10

35
Q

Main activities of thrombin?

A

Activate platelets

Stabilize fibrin

36
Q

Coumadin (warfarin) inhibits?

A

Vitamin K - cannot activate factors 2, 7, 9, 10

37
Q

The _____ can regulate clot formation and dissolution

A

Endothelium

38
Q

What 3 things can the Endothelium produce to INHIBIT platelets?

A
  1. Adenosine DisphophatASE - blocks ADP which activates platelets
  2. NO
  3. Prostacyclins
39
Q

What can the Endothelium produce to break down fibrin?

A

Tissue Plasminogen Activator (t-PA)

40
Q

How does Tissue Plasminogen Activator (t-PA) break down fibrin?

A

It activates Plasmin!

Plasmin then breaks apart Fibrin and degrades the clot

41
Q

Cascade of events of the fibrinolytic activity of the Endothelium

A
  • Endothelium produces t-PA
  • t-PA activates Plasmin
  • Plasmin breaks Fibrin apart and degrades clot
42
Q

What inhibits plasmin?

A

Alpha2 - antiplasmin – keeps clot stable

43
Q

What receptors on the endothelium can bind Thrombin and exert anti-coagulation effects?

A

Thrombomodulin

44
Q

Once Thrombomodulin binds Thrombin, then what happens?

A

Activates protein C and S which INHIBIT factors 5 and 8

= Anticoagulation

45
Q

Heparin-like molecules on the endothelial surface activate _____ which inhibits ______

A

Antithrombin III

Thombin

46
Q

Small bleeds (petechiae and purpura) are due to defects in?

A

Primary hemostasis

47
Q

How do defects in primary hemostasis present?

A

Nosebleeds
Excessive menstruation
GI bleeds

48
Q

Bleeds in joints (hemarthrosis) are due to defects in?

A

Secondary hemostasis

49
Q

Secondary hemostasis defects cause?

A

Bleeds in joints (hemarthrosis)

50
Q

Generalized defects of small vessels cause?

A

Eccyhmoses

MOD (68 decks)

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