Haemostasis: Flashcards

1
Q

What is haemostasis?

A

Prevents and stops bleeding

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2
Q

How quickly after injury does hemostasis occur?

A

Seconds to hours

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3
Q

What are the three main processes in hemostasis?

A

Vasoconstriction, platelet aggregation, leucocyte migration

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4
Q

What happens when there is too little hemostasis?

A

Excessive bleeding, clotting defects and platelet deficiency

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5
Q

What happens if there is too much hemostasis?

A

Thrombus formation, atherosclerosis, septicemic shock

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6
Q

How many platelets are in a ml of blood?

A

250 million

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7
Q

What is thrombocytopenia?

A

Struggle with blood clotting

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8
Q

What happens to the structure of a platelet when it is activated?

A

Morphological change - changes from a smooth to rough surface with extensions due to rearrangement of actin and myosin

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9
Q

How are platelets activated?

A
  • Platelets adhere to damaged collagen
  • Binding sites include involvement of von Willebrand factor (vWF)
  • vWF released from endothelial cells and present in plasma
  • Platelets become activated
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10
Q

How is platelet activation an example of positive feedback?

A

Activated platelets release biochemicals into area for increased vasoconstriction, which results in more collagen being exposed and more platelets being activated

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11
Q

What does ADP do in platelet plug formation?

A

Makes platelets sticky

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12
Q

What does serotonin do in platelet plug formation?

A

Activates vasoconstriction

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13
Q

What does thromboxane A2 do in platelet plug formation?

A

It is a prostaglandin - vasoconstrictor and activates

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14
Q

How does a platelet plug form?

A
  • Adhesion, activation, aggregation
  • ADP makes platelets sticky
  • Serotonin activates vasoconstriction
  • Thromboxane A2 is a prostaglandin - vasoconstricts and activates
  • Platelet adhesion activates platelets (morphological and biological change)
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15
Q

What is a platelet plug?

A

Cell fragments of megakaryotes present in the blood with no nucleus/organelles/DNA/proteins

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16
Q

What are the two pathways in the coagulation cascade?

A

Intrinsic and extrinsic

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17
Q

When is the intrinsic pathway triggered?

A

When blood in cells is exposed to collagen

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18
Q

Why must venepuncture test tubes be coated with anti-coagulant?

A

To stop initiation of the intrinsic pathway

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19
Q

Where does the extrinsic pathway occur?

A

Tissues

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20
Q

What is factor 13 activated by?

A

Thrombin

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21
Q

What happens during the intrinsic pathway?

A

Co-factors 12, 11 and 9 are activated which converts 10 to its active form

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22
Q

What does thrombin do?

A

Converts fibrinogen to fibrin to form a mesh

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23
Q

Do RBCs contribute to the hemostasis process?

A

No

24
Q

Where is fibrinogen produced?

A

Liver

25
Q

Describe the process of the final common pathway in the coagulation cascade

A

Prothrombin activator converts prothrombin to thrombin
Reaction requires calcium
Thrombin converts fibrinogen into fibrin
This forms cross-linked fibrin clot

26
Q

What happens during the intrinsic pathway?

A

Activated by contact with a damaged surface

factor XII - factor XI - factor IX (+factor VIII and vWF)

27
Q

What happens during the extrinsic pathway?

A

Activated by release fo tissue factors

Factor VII - common pathway

28
Q

What does prostacyclin do?

A

From intact endothelium, inhibits platelet adhesion and aggregation

29
Q

What does nitro oxide do?

A

From intact endothelium inhibits platelet adhesion

30
Q

How does the liver assist with clotting?

A

Synthesises clotting factors and bile salts

31
Q

What do bile salts do?

A

Increase rate of uptake of vitamin K from GI tract and move it to blood

32
Q

What does warfarin do?

A

Vit K antagonist

Anticoagulant

33
Q

How is a clot removed?

A
  • Cell growth and cell division repairs damaged vessel
  • Clot retracts and dissolves
  • Plasmin (an enzyme) trapped in the clot acts on fibrin to break it into soluble fragments
  • Plasmin takes around a week to act
34
Q

How is plasmin made?

A

Plasminogen reacts with TPA

35
Q

How does the endothelium prevent clot formation?

A

Intact it separates collagen, tissue factors and vWF

36
Q

How does glycocalyx prevent clot formation?

A

Inhibits adhesion of platelets

37
Q

How do prostacyclin and nitric oxide prevent clot formation?

A

Inhibits platelet activation and aggregation

38
Q

How do CD39 and ecto-ADPases prevent clot formation?

A

Metabolize ADP

39
Q

How does TPA prevent clot formation?

A

Dissolves fibrin

40
Q

How does heparin sulphate prevent clot formation?

A

Co-factor for antithrombin

41
Q

Why is antithrombin an anti-coagulant?

A

Inactivates thrombin

Inactivates factor Xa and IXa

42
Q

Which factors do coumarin drugs impact?

A

II, VII, IX and X

43
Q

What is a thromboembolism?

A

Abnormal clot formation

44
Q

What is a thrombus?

A

Clot attached to vessel

45
Q

What is an emboli?

A

Free-floating clots

46
Q

Examples of anti platelet drugs

A

Aspirin, clopidogrel

47
Q

Examples of anticoagulant drugs

A

Warfarin, heparin

48
Q

Examples of fibrinolytic drugs

A

Urokinase, streptokinase, genetically engineered tissue plasminogen activator (t-PA)

49
Q

Why should aspirin not be taken before surgery?

A

Reduces platelets binding to sub-endothelial components
Impairs platelet aggregation
Prolongs bleeding

50
Q

Where is heparin used?

A

Catheters, dialysis, heart-lung machines

51
Q

Examples of calcium ion reducers

A

EDTA, citrate, oxalate

52
Q

What do siliconised containers do?

A

Reduce platelet activation

53
Q

Processes inside haemostasis

A

Vasoconstriction
Platelet aggregation
Leucocyte migration

54
Q

Processes inside inflammation

A

Early = neutrophil, late = macrophage
Chemoattractant release
phagocytosis

55
Q

Processes inside proliferation

A

Collagen and ECM synthesis
Angiogenesis
Fibroblast proliferation
Granulation tissue formation

56
Q

Processes inside remodelling

A

Epithelialisation
ECM remodelling
Increase in wound strength