Week 28 / Haemostasis 2 Flashcards
Q: How is the coagulation cascade traditionally divided?
A: The coagulation cascade is traditionally divided into 3 interacting pathways:
Intrinsic Pathway : Slow responding
Extrinsic Pathway : Quick responding
Common Pathway
Q: What is unique about the Intrinsic Pathway?
A: The Intrinsic Pathway involves all components present in the bloodstream.
Q: What is unique about the Extrinsic Pathway?
A: The Extrinsic Pathway requires a factor (usually tissue factor) that is not normally present in the bloodstream.
Q: What happens after both the Intrinsic and Extrinsic Pathways?
A: Both the Intrinsic and Extrinsic Pathways converge on and activate the Common Pathway.
Q: When does the Extrinsic Pathway of the coagulation cascade begin?
A: The Extrinsic Pathway begins when damage occurs to the surrounding tissues, such as in a traumatic injury.
Q: What factors are involved in the Extrinsic Pathway of the coagulation cascade?
A: The Extrinsic Pathway involves Tissue Factor (TF), Factor VII, and Calcium ions (Ca²⁺).
Q: What is the role of Tissue Factor (TF) in the coagulation cascade?
A: Tissue Factor (TF), also known as Factor III, is the principal initiator of coagulation in vivo. It is a cell-bound glycoprotein expressed in extravascular tissues like fibroblasts and smooth muscle cells, and is exposed to blood when the endothelial barrier is breached.
Q: What happens when damaged extravascular cells come into contact with blood?
A: Damaged extravascular cells release Tissue Factor (TF), which triggers the coagulation cascade.
Q: What complex is formed when Tissue Factor (TF) interacts with Factor VII and Calcium ions (Ca²⁺)?
A: The Tissue Factor (TF)-FVIIa complex is formed, which is known as the extrinsic tenase and acts as the Factor X activator in the extrinsic pathway.
Q: What is the role of the TF-FVIIa complex in the coagulation cascade?
A: The TF-FVIIa complex activates Factor X of the Common Pathway, leading to thrombin (FIIa) generation, and can also activate Factor IX of the Intrinsic Pathway (also known as the “alternate pathway”).
Q: What triggers the Intrinsic Pathway of the coagulation cascade?
A: The Intrinsic Pathway begins when blood comes into contact with collagen in a damaged blood vessel wall.
Q: What is the initial complex formed in the Intrinsic Pathway?
A: Factor XII (FXII) forms a complex with high-molecular-weight kininogen (HMWK) and prekallikrein on collagen, leading to the activation of FXII.
Q: How is Factor XI activated in the Intrinsic Pathway?
A: FXIIa activates Factor XI, which in turn activates Factor IX.
Q: What forms the intrinsic tenase complex and what is its role?
A: The intrinsic tenase complex consists of Factor IXa, Factor VIIIa, Calcium ions (Ca²⁺), and phosphatidylserine. It activates Factor X in the Common Pathway, leading to thrombin generation.
Q: What is the purpose of the Common Pathway in the coagulation cascade?
A: The Common Pathway produces fibrin to help seal off the breach in the blood vessel wall.
5 different steps of common pathway
Flashcard 2
Q: What activates the Common Pathway?
Flashcard 3
Q: What is the first step in the Common Pathway?
Flashcard 4
Q: What happens after Factor X is activated in the Common Pathway?
Flashcard 5
Q: What does thrombin (FIIa) do in the Common Pathway?
Flashcard 6
Q: What occurs after fibrinogen is converted to fibrin?
Flashcard 7
Q: What stabilizes the fibrin network in the Common Pathway?
A: Both the Intrinsic and Extrinsic pathways activate the Common Pathway.
A: The activation of Factor X (FX).
A: Prothrombin (FII) is converted into thrombin (FIIa).
A: Thrombin cleaves fibrinogen (FI) to produce fibrin (F1a).
A: Fibrin polymerizes and forms a network to help seal the wound.
A: Factor XIIIa cross-links and stabilizes the fibrin polymers.
Q: How is Factor X (FX) activated in the Common Pathway?
A: Factor X is activated by the extrinsic and intrinsic tenase complexes of the Extrinsic and Intrinsic Pathways.
Q: What forms after Factor Xa activation in the Common Pathway?
A: Factor Xa forms a complex with Factor Va, Ca²⁺, and phosphatidylserine, known as the “prothrombinase” complex.
Q: What does the prothrombinase complex do?
A: The prothrombinase complex converts prothrombin (FII) into thrombin (FIIa).
Q: What does thrombin (FIIa) do in the Common Pathway?
A: Thrombin (FIIa) cleaves fibrinogen (FI) into fibrin monomers.
Q: What happens to fibrin monomers after cleavage by thrombin?
A: Fibrin monomers undergo spontaneous polymerization.
Q: How is the fibrin network stabilized in the Common Pathway?
A: Factor XIIIa induces cross-linking and stabilization of the fibrin polymers.
Q: What is a major limitation of the Coagulation Cascade Model?
A: The model doesn’t fully explain how blood clots in vivo, as it assumes that the intrinsic and extrinsic pathways are independently capable of initiating clot formation.
Q: What happens if there is a deficiency in the initial components of the intrinsic pathway (FXII, HMWK, or prekallikrein)?
A: A deficiency in the initial components of the intrinsic pathway does not lead to a bleeding tendency.
Q: What happens in Factor VIII or Factor IX deficiency?
A: Factor VIII or Factor IX deficiency leads to a serious bleeding tendency, even though the extrinsic pathway is intact.
Q: What happens in Factor VII deficiency?
A: Factor VII deficiency leads to a serious bleeding tendency, even though the intrinsic pathway is intact.
Q: What are the distinct, but overlapping, steps in secondary haemostasis according to the modern cell-based model?
A: The steps are Initiation, Amplification, and Propagation.
Q: What two cell types are involved in the process of secondary haemostasis?
A: The two cell types involved are Tissue factor (TF)-bearing cells and Platelets.
Q: How are the two cell types (TF-bearing cells and platelets) involved in secondary haemostasis kept apart?
A: The two cell types are kept apart until vascular injury occurs.
OPEN PP FOR Secondary Haemostasis – Cell-Based Model
OPEN PP FOR Secondary Haemostasis – Cell-Based Model
Q: What is fibrinolysis?
A: Fibrinolysis is the process that dissolves and removes the fibrin clot following secondary haemostasis.
Q: What is the main enzyme involved in fibrinolysis?
A: The main enzyme involved is plasmin, a proteolytic enzyme that degrades the fibrin mesh.
Q: What are the key steps involved in fibrinolysis?
A: The key steps include the release of plasminogen activators, conversion of plasminogen to plasmin, and clot lysis with the release of degradation products.
Q: What does fibrinolysis ensure after a clot is formed?
A: It ensures the localisation of fibrin clot formation and the removal of the clot after wound healing.
Q: Why is regulation of haemostasis important?
A: It ensures that primary and secondary haemostasis are restricted to the local site of vascular injury and prevents excessive clot formation while maintaining blood vessel patency.
Q: How must the size of the primary and secondary haemostatic plugs be regulated?
A: The size must be restricted to keep the blood vessel open (patent) and prevent obstruction.
Q: Why is the fibrinolytic system regulated?
A: It must be regulated to ensure the removal of unwanted fibrin clots while preserving fibrin in wounds for proper healing.
Q: How is haemostasis regulated?
A: Haemostasis is regulated through a combination of multiple endogenous antithrombotic and antifibrinolytic systems.
