1
Q
what is haemostasis?
A
- process that maintains fluid state of blood in normal vessels yet still allowing clot formation at site of injury acting with thrombosis.
2
Q
what are the 3 components of haemostasis?
A
- vasoconstriction to prevent blood loss, platelet plug formation and coagulation cascade.
3
Q
what are platelets?
A
- anucleate buddings of megakaryocytes cytoplasm that is responsible for primary haemostasis.
- 7 to 10 day lifespan.
4
Q
how do platelets react to vessel injury?
A
- platelet adhesion : adheres to collagen via WF receptor when exposure of underlying tissue occurs.
- platelet activation and secretion : of alpha granules and dense granules to attract more platelets.
- platelet aggregation : cross-linking to form insoluble platelet plug to provide stability. platelets contract.
5
Q
briefly describe the three pathways of the coagulation cascade. ( extrinsic, intrinsic and common pathway)
A
- extrinsic is shorter and faster : tissue damage activates F3 which along with calcium and F7 activate tissue factor complex.
- intrinsic pathway starts with F12 activated by exposure to collagen which along with PF3 released by platelets, calcium, F8+9 activate factor X activator complex.
- the factor X activator and tissue factor complexes activate FX to activate prothrombin activator to activate thrombin which converts fibrinogen to insoluble fibrin to form mesh.
6
Q
how is coagulation measured in blood tests?
A
- APTT : to measure time for intrinsic pathway, prolonged suggests deficiencies in F8, 9, 11 , 12.
- PT : extrinsic time indicator, prolonged due to F7 deficiency,
- if APTT & PT both prolonged deficiencies in F5,10, thrombin and fibrinogen.
- TCT : conversion of fibrin via thrombin action measure.
7
Q
what are some factors that oppose clot formation?
A
- Tissue factor pathway inhibitor : in extrinsic pathway binds to F7 inhibiting ability to activate F10.
- thrombin : binds to thrombomodulin receptors in endothelium eliminating thrombins clot producing effects binding protein c + s. inactivates F8 and 5.
- antithrombin iii : inactivates thrombin, activated by heparin, prevents spread of clot.
8
Q
breifly putline the fibrinolytic pathway.
A
- plasminogen activator causes activation of plasmin from plasminogen which breaks fibrin into d-dimers detected in blood.
9
Q
what is thrombocytopenia?
A
- deficiency of platelets in blood resulting in bleeding into tissues bruising and slow blood clotting after injury.
- present with purpura, petechia, mucosal bleed, menorrhagia or epistaxis.
10
Q
what causes thrombocytopenia?
A
- decreased production due to sepsis, B12 deficiency, marrow aplasia.
- increased consumption due to hypersplenism etc.
11
Q
what are some acquired disorders of coagulation?
A
- Disseminated intravascular coagulation.
- liver disease.
- Vitamin K deficiency.
- warfarin.
12
Q
what is von willebrand’s disease?
A
- autosomal dominant inherited bleeding disorder.
- vWF needed in the coagulation process deficient or defective causing extreme bleeding under stress.
- platelet count normal but defective in type 2, type 1 and 3 reduced quality.
13
Q
what is haemophilia A?
*X linked recessive.
A
- F8 deficiency affecting intrinsic pathway.
- easy bruising, massive haemorrhage in operative procedures, petechiae present.
- APTT prolonged but normal PT.
- treated with infusions of recombinant F8.
14
Q
what is haemophilia B?
*X linked recessive.
A
- severe F9 deficiency clinically indistinguishable from haemophilia A.
- prolonged APTT and normal PT.
- treated with infusions of recombinant F9.
15
Q
what is Disseminated intravascular coagulation?
A
- excessive activation of coagulation which leads to formation of microthrombi in microvasculature.
- consequence there is a consumption of platelets, fibrin and coagulation factors to make clots which causes haemorrhage by depletion eventually.
- hypoxia and infarction do to the thrombi.
16
Q
what causes DIC?
A
- sepsis, surgery, trauma, cancer, pregnancy complications.
PP
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