Haemostasis Flashcards

1
Q

Haemostasis 3 processes

A

Vasoconstriction
Formation of unstable platelet plug at site of vessel wall damage (primary haemostasis)
Formation of a stable fibrin clot (secondary haemostasis/coagulation)

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2
Q

Platelet definition

A

Discoid,non nucleated, granule containing cells
Derived from myeloid SCs

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3
Q

Platelet lifespan

A

10 days

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4
Q

How to platelets become activated

A

Following injury to vessel walls platelets stick to damaged endothelium to collagen. The adhesion of platelets causes them to activate and changes their shape from a disc to a more rounded form with spicules to encourage platelet-platelet interaction

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5
Q

3 Important components of platelet granules released

A

ADP
fibrinogen
Von Willebrand factor

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6
Q

Thromboxane 2 function

A

Vasoconstriction
Platelet aggregation

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7
Q

What produces thromboxane A2

A

Platelets

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8
Q

What 2 chemicals have +ve feedbacks on platelet recruitment activation and aggregation
How

A

ADP and thromboxane A2 binding respectively to P2Y12 and thromboxane A2 receptors on platelets

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9
Q

Fibrinogen role

A

Binds to GPIIb/IIIa receptors which further activates platelets
Linking platelets together to form platelet plug

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10
Q

Aspirin mechanism

A

Inhibits production of thromboxane A2 by irreversibly (effects last till platelets are replaced~7days) blocking action of cyclo-oxygenase resulting in reduced platelet aggregation.

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11
Q

Clopidogrel

A

Irreversibly blocking p2y12 (ADP) receptor on platelets.
Last 7 days

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12
Q

Von Willebrand Factor (VWF)

A

Glycoprotein synthesised by endothelial cells and megakaryocytes. Circulates in plasma. Mediates adhesion of platelets to sites of injury and promotes platelet aggregation

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13
Q

site of majority of clotting factor production

A

Liver

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14
Q

How is coagulation initiated

A

A tissue factor (TF) mainly located on sites not usually exposed to blood. Interaction between blood and TF leads to activation of prothrombin and an initial small amount of thrombin.

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15
Q

Amplification phase

A

Small amount of thrombin mediates activation of co-factors, zygomen (preenzyme) factor XI and platelets

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16
Q

Propagation Phase

A

Factors cause +ve feedback loop consequently causing rapid burst in thrombin propagation