Haemostasis: Flashcards

(56 cards)

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?

24
Q

Where is fibrinogen produced?

25
Describe the process of the final common pathway in the coagulation cascade
Prothrombin activator converts prothrombin to thrombin Reaction requires calcium Thrombin converts fibrinogen into fibrin This forms cross-linked fibrin clot
26
What happens during the intrinsic pathway?
Activated by contact with a damaged surface | factor XII - factor XI - factor IX (+factor VIII and vWF)
27
What happens during the extrinsic pathway?
Activated by release fo tissue factors | Factor VII - common pathway
28
What does prostacyclin do?
From intact endothelium, inhibits platelet adhesion and aggregation
29
What does nitro oxide do?
From intact endothelium inhibits platelet adhesion
30
How does the liver assist with clotting?
Synthesises clotting factors and bile salts
31
What do bile salts do?
Increase rate of uptake of vitamin K from GI tract and move it to blood
32
What does warfarin do?
Vit K antagonist | Anticoagulant
33
How is a clot removed?
- 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
How is plasmin made?
Plasminogen reacts with TPA
35
How does the endothelium prevent clot formation?
Intact it separates collagen, tissue factors and vWF
36
How does glycocalyx prevent clot formation?
Inhibits adhesion of platelets
37
How do prostacyclin and nitric oxide prevent clot formation?
Inhibits platelet activation and aggregation
38
How do CD39 and ecto-ADPases prevent clot formation?
Metabolize ADP
39
How does TPA prevent clot formation?
Dissolves fibrin
40
How does heparin sulphate prevent clot formation?
Co-factor for antithrombin
41
Why is antithrombin an anti-coagulant?
Inactivates thrombin | Inactivates factor Xa and IXa
42
Which factors do coumarin drugs impact?
II, VII, IX and X
43
What is a thromboembolism?
Abnormal clot formation
44
What is a thrombus?
Clot attached to vessel
45
What is an emboli?
Free-floating clots
46
Examples of anti platelet drugs
Aspirin, clopidogrel
47
Examples of anticoagulant drugs
Warfarin, heparin
48
Examples of fibrinolytic drugs
Urokinase, streptokinase, genetically engineered tissue plasminogen activator (t-PA)
49
Why should aspirin not be taken before surgery?
Reduces platelets binding to sub-endothelial components Impairs platelet aggregation Prolongs bleeding
50
Where is heparin used?
Catheters, dialysis, heart-lung machines
51
Examples of calcium ion reducers
EDTA, citrate, oxalate
52
What do siliconised containers do?
Reduce platelet activation
53
Processes inside haemostasis
Vasoconstriction Platelet aggregation Leucocyte migration
54
Processes inside inflammation
Early = neutrophil, late = macrophage Chemoattractant release phagocytosis
55
Processes inside proliferation
Collagen and ECM synthesis Angiogenesis Fibroblast proliferation Granulation tissue formation
56
Processes inside remodelling
Epithelialisation ECM remodelling Increase in wound strength