Session 14: Blood groups Flashcards
Why do we clot?
- Primary haemostasis prevents us from, bleeding
- Sealing vascular defect is an NB immunological
function - Intact endothelium maintains an adequate barrier
between tissue and blood
Name the five main factors responsible for haemostasis.
- Endothelium
- Platelets and Von Willebrand factor (primary
haemostasis) - Procoagulant
- Anticoagulants
- Fibrinolysis
Name the three endothelium PROCOAGULANT functions and briefly describe each in terms of vessel damage.
- VASOCONSTRICTION
- endothelium releases endothelin-1 that causes
vasoconstriction - vasoconstriction has an immediate effect on blood
loss and also brings platelets to the walls of the
damaged vessel - EXPOSURE OF COLLAGEN
- collagen facilitates the binding of platelets and
and Von Willbrand factor to injured vessels wall - platelets are aggregated form a primary haemostatic plug and
participate in secondary haemostasis - EXPOSURE OF TISSUE FACTOR
- initiates the coagulation cascade
Name the three endothelium ANTICOAGULANT functions and briefly describe each in terms of an intact vessel.
- VASODILATION
- mediated by NO and prostacyclin produced by intact endothelium
- INHIBITS PLATELET AGGREGATION
- NO is a direct inhibitor of platelet aggregation
- “hides” collagen
- expresses CD39 that inhibits aggregation
- INHIBITS COAGULATION CASCADE
- “hides” tissue factor from circulating procoagulants
- houses many anticoagulant proteins and receptors
Describe the platelet structure.
- Anucleate
- Glycoprotein receptors that bind fibrinogen, VWF, and
the vessel wall - Internal structure made of contractile protein and
granules
What is the function of the platelet?
Formation of primary haemostatic plug at side of vessel damage, achieved through: * adhesion * aggregation * release reactions and amplifications
Describe the process of adhesion in the functioning of platelets.
- VWF adheres to exposed collagen - Platelets bind to VWF via GPIb receptor - Platelets adhere to damaged vessel wall - Binding of VWF to platelets activates platelets to perform further functions - Platelets undergo shape changes called platelet spreading - Increases the platelets SA
Describe the 3 functions of the Von Willebrand Factor.
- Involved in platelet adhesion to collagen - Involved in platelet aggregation - Carries and extends the half-life of factor VIII
Describe the aggregation process in the functioning of platelets.
- Activated platelets upregulate GPIIbIIIa receptors - GPIIbIIIa receptors bind fibronogen/VWF then bind to other platelets= aggregration - Fibronogen and VWF bridge between platelets and GPIIbIIIa receptors
Describe release reactions and amplification in the functioning of platelets.
- Once activated, platelets are triggered to release granule content - The granule content is involved in further auto- activation - Additional platelets accumulate, become activated and adhere to each other
Discuss the platelet plug.
- Sufficient to immediately seal vessel damage - Not stable, needs reinforcement - Reinforced by fibrin
Describe coagulation.
* Coagulating factors are precursor proteins * When needed, they're activated in a sequential cascade and controlled by a negative feedback * Cascade culminates generation of thrombin * Thrombin converts fibrinogen to fibrin * Fibrin enmeshes aggregated platelets and converts unstable platelet plugs to stable haemostatic plug
Name the 2 types of cascade models and where they’re used.
- Laboratory-based cascade
(old) - Cell-based cascade (new)
Explain how regulators of coagulation (anticoagulants) work.
- Natural anticoagulants regulate extent to which coagulation occurs - Assures coagulation doesn't progress beyond damaged site/ becomes pathological thrombosis - If clotting switch is "on", anticoagulation switches are "off"
Define fibrinolysis and its importance.
Definition: process of removal of fibrin meshwork
Importance: tissue remodeling and restoring vessel patency
- complex balance between initiators and inhibitors
- fibrinolysis and its protein roll players act w/ fibrin to perform its function- fibrin orchestrates its own destruction
