Introduction To Haemostasis

Primary Haemostasis = [blank_start]Formation of Platelet Plug[blank_end] Secondary Haemostasis = [blank_start]Formation of Fibrin Clot[blank_end]

Platelets are formed on the surface of which type of cell? [blank_start]Megakaryocyte[blank_end]

As a platelet has a lifespan of [blank_start]7-10 days[blank_end], a patient on e.g. aspirin should have this medication stopped this period of time before surgery to avoid any unnecessary bleeding.

Platelets are formed on the surface of megakaryocytes which are found within the bone marrow

Von Willebrand Factor binds to Factor [blank_start]VIII[blank_end] in the circulation. Without WVF the aforementioned factor would be broken down in the blood.

Factor VIII is released from Von Willebrand Factor by action of [blank_start]Thrombin[blank_end] (Factor [blank_start]IIa[blank_end])

Von Willebrand factor also forms part of the platelet mesh that forms in response to bleeding, holding the platelets together.

Reduced number of platelets in the blood is known as [blank_start]thrombocytopenia[blank_end]

The commonest inherited bleeding disorder is a deficiency of [blank_start]Von Willebrand Factor[blank_end]

Which usually results in a more serious bleed?

Failure of primary haemostasis typically causes which 3 of the following?

If you were concerned about the failure of primary haemostasis you would check the [blank_start]platelet[blank_end] count in the blood.

Coagulation Cascade (1): Tissue Factor binds with Factor [blank_start]VIIa[blank_end]

Coagulation Cascade (2): TF-VIIa Complex activates Factor [blank_start]X[blank_end] to Factor [blank_start]Xa[blank_end]. In the meantime, TF-VIIa also activates Factor [blank_start]IX[blank_end] to Factor [blank_start]IXa[blank_end]. This Factor then binds with Factor [blank_start]VIIIa[blank_end] and this complex then also activates Factor [blank_start]X[blank_end] to Factor [blank_start]Xa[blank_end]

Coagulation Cascade (3): Factor Xa then binds with Factor [blank_start]Va[blank_end] to form the enzyme [blank_start]prothrombinase[blank_end], which facilitates the conversion of [blank_start]Prothrombin[blank_end] (Factor [blank_start]II[blank_end]) to [blank_start]Thrombin[blank_end] (Factor [blank_start]IIa[blank_end])

Coagulation Cascade (4): Thrombin (Factor IIa) then goes about activating Factor [blank_start]VIII[blank_end] to Factor [blank_start]VIIIa[blank_end], in turn releasing it from its binding to [blank_start]Von Willebrand Factor[blank_end], whilst also activating Factor [blank_start]V[blank_end] to Factor [blank_start]Va[blank_end]

Coagulation Cascade (5): The main function of Thrombin, however, is in the activation of [blank_start]Fibrinogen[blank_end] (Factor I) to [blank_start]Fibrin[blank_end] (Factor Ia).

Coagulation Cascade (6): Finally, soluble Fibrin produced by thrombin-mediated activation is organised into crosslinked Fibrin by action of Factor [blank_start]VIIIa[blank_end]

Fibrin is broken down into Fibrin Degradation Products (e.g. D-dimers) via which enzyme? [blank_start]Plasmin[blank_end]

Plasminogen --> Plasmin is mediated by which enzyme, which is thus used clinically as a thrombolytic agent? [blank_start]Tissue Plasminogen Activator[blank_end]

Screening tests for Fibrin Clot Formation: [blank_start]Prothrombin Time[blank_end]: Tests TF-VIIa complex activating factor X so that the Xa/Va complex (prothrombinase) can be produced. [blank_start]Activated Partial Thromboplastin Time[blank_end]: Tests VIIIa/IXa complex activating Factor X so that the Xa/Va complex (prothrombinase) can be produced.

Anti-Thrombin III binds to ... thus inhibiting secondary haemostasis

Thrombin can bind to an endothelial cell forming thrombomodulin, which in turn activates Protein [blank_start]C[blank_end] and Protein [blank_start]S[blank_end] (give in alphabetical order).

Proteins C & S affect which complexes?

Deficiency of clotting factors is called [blank_start]haemophilia[blank_end] Increased tendency to form clots is called [blank_start]thrombophilia[blank_end]