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Questions and Answers
The coagulation cascade is traditionally divided into 4 interacting pathways – intrinsic, extrinsic, common, and unique pathways.
The coagulation cascade is traditionally divided into 4 interacting pathways – intrinsic, extrinsic, common, and unique pathways.
False (B)
The intrinsic pathway involves reactions with a specific group of clotting factors that are only present in the blood stream.
The intrinsic pathway involves reactions with a specific group of clotting factors that are only present in the blood stream.
True (A)
The extrinsic pathway requires a factor that is normally present in the blood.
The extrinsic pathway requires a factor that is normally present in the blood.
False (B)
Both the intrinsic and extrinsic systems eventually converge on and activate the intrinsic pathway.
Both the intrinsic and extrinsic systems eventually converge on and activate the intrinsic pathway.
The Extrinsic Pathway begins when damage occurs to the surrounding tissues.
The Extrinsic Pathway begins when damage occurs to the surrounding tissues.
The principal initiator of coagulation in vivo is tissue factor (TF).
The principal initiator of coagulation in vivo is tissue factor (TF).
TF-FVIIa complex activates Factor VIII of the Intrinsic Pathway.
TF-FVIIa complex activates Factor VIII of the Intrinsic Pathway.
The Extrinsic Pathway involves interaction between tissue factor (as cofactor), FVII and Ca++.
The Extrinsic Pathway involves interaction between tissue factor (as cofactor), FVII and Ca++.
The Intrinsic Pathway begins when blood comes into contact with collagen in damaged blood vessel wall.
The Intrinsic Pathway begins when blood comes into contact with collagen in damaged blood vessel wall.
Both intrinsic & extrinsic pathways activate the common pathway, resulting in production of fibrin to seal off the breach in blood vessel wall.
Both intrinsic & extrinsic pathways activate the common pathway, resulting in production of fibrin to seal off the breach in blood vessel wall.
Traditional Coagulation Cascade Model fully explains how blood clots in vivo.
Traditional Coagulation Cascade Model fully explains how blood clots in vivo.
Factor VIII or IX deficiency leads to a serious bleeding tendency, although the extrinsic pathway is intact.
Factor VIII or IX deficiency leads to a serious bleeding tendency, although the extrinsic pathway is intact.
Secondary haemostasis occurs in distinct, but non-overlapping, steps: Initiation, Amplification, and Propagation.
Secondary haemostasis occurs in distinct, but non-overlapping, steps: Initiation, Amplification, and Propagation.
Fibrinolysis is the process that dissolves & removes the fibrin clot following secondary haemostasis.
Fibrinolysis is the process that dissolves & removes the fibrin clot following secondary haemostasis.
The size of both the primary & secondary hemostatic plugs must be restricted to keep blood vessel patent.
The size of both the primary & secondary hemostatic plugs must be restricted to keep blood vessel patent.
Endothelium is a physiological regulator of global hemostasis by acting as a physical barrier.
Endothelium is a physiological regulator of global hemostasis by acting as a physical barrier.
Surface heparin-like glycosaminoglycans (GAGs) enhance ATIII & TFPI activity in primary hemostasis.
Surface heparin-like glycosaminoglycans (GAGs) enhance ATIII & TFPI activity in primary hemostasis.
Plasminogen activator inhibitor-1 is produced in the liver.
Plasminogen activator inhibitor-1 is produced in the liver.
Antithrombin III inhibits only factor VIIa.
Antithrombin III inhibits only factor VIIa.
Protein C is activated by heparin.
Protein C is activated by heparin.
Protein S is produced in endothelial cells.
Protein S is produced in endothelial cells.
Thrombin-activatable Carboxypeptidase B binds to lysine residues in fibrin, promoting plasminogen binding and activation.
Thrombin-activatable Carboxypeptidase B binds to lysine residues in fibrin, promoting plasminogen binding and activation.
Plasminogen activator binds and inactivates tissue plasminogen activator.
Plasminogen activator binds and inactivates tissue plasminogen activator.
Alpha2-Antiplasmin is produced in the liver.
Alpha2-Antiplasmin is produced in the liver.
Polyphosphates form a loose fibrin network that is easily degraded by plasmin.
Polyphosphates form a loose fibrin network that is easily degraded by plasmin.
Extracellular nuclear material promotes fibrin degradation.
Extracellular nuclear material promotes fibrin degradation.
Plasminogen activator inhibitor-1 complex is not inhibited by thrombin-thrombomodulin.
Plasminogen activator inhibitor-1 complex is not inhibited by thrombin-thrombomodulin.
Which pathway requires a factor that is not normally present in the blood?
Which pathway requires a factor that is not normally present in the blood?
Which pathway involves interactions between tissue factor, Factor VII, and Ca++?
Which pathway involves interactions between tissue factor, Factor VII, and Ca++?
Which factor deficiency leads to a serious bleeding tendency, although the extrinsic pathway is intact?
Which factor deficiency leads to a serious bleeding tendency, although the extrinsic pathway is intact?
What are the components involved in the Common pathway?
What are the components involved in the Common pathway?
What is true about the Intrinsic pathway?
What is true about the Intrinsic pathway?
What promotes plasminogen binding and activation by binding to lysine residues in fibrin?
What promotes plasminogen binding and activation by binding to lysine residues in fibrin?
Which physiological regulator inhibits the TF-FVIIa & TF-FVIIaFXa complexes?
Which physiological regulator inhibits the TF-FVIIa & TF-FVIIaFXa complexes?
What is the mechanism of action of Thrombin-activatable Carboxypeptidase B (TAFI)?
What is the mechanism of action of Thrombin-activatable Carboxypeptidase B (TAFI)?
What is the role of Plasminogen activator inhibitor-1 (PAI-1) in fibrinolysis?
What is the role of Plasminogen activator inhibitor-1 (PAI-1) in fibrinolysis?
What is the function of Extracellular nuclear material in the context of haemostasis?
What is the function of Extracellular nuclear material in the context of haemostasis?
What is the role of Alpha2-Antiplasmin in haemostasis?
What is the role of Alpha2-Antiplasmin in haemostasis?
Which physiological regulator is a cofactor for both Thrombin-activatable Carboxypeptidase B (TAFI) & activated protein C?
Which physiological regulator is a cofactor for both Thrombin-activatable Carboxypeptidase B (TAFI) & activated protein C?
Which physiological regulator is enhanced by heparin (exogenous) & heparin-like glycosaminoglycans (GAGs) on endothelial cells?
Which physiological regulator is enhanced by heparin (exogenous) & heparin-like glycosaminoglycans (GAGs) on endothelial cells?
What is the function of Polyphosphates released from dense granules in platelets during activation?
What is the function of Polyphosphates released from dense granules in platelets during activation?
What is the role of Protein C in haemostasis?
What is the role of Protein C in haemostasis?
What does the Thrombin-activatable Carboxypeptidase B (TAFI) bind to, promoting fibrinolysis?
What does the Thrombin-activatable Carboxypeptidase B (TAFI) bind to, promoting fibrinolysis?
What is the principal initiator of coagulation in vivo?
What is the principal initiator of coagulation in vivo?
Which of the following forms a primary complex with high-molecular-weight kininogen (HMWK) & prekallikrein on collagen in the Intrinsic Pathway?
Which of the following forms a primary complex with high-molecular-weight kininogen (HMWK) & prekallikrein on collagen in the Intrinsic Pathway?
Which of the following pathways is slower-responding and begins when blood comes into contact with collagen in damaged blood vessel wall?
Which of the following pathways is slower-responding and begins when blood comes into contact with collagen in damaged blood vessel wall?
Which pathway involves interactions between tissue factor (as cofactor), Factor VII, and Ca++?
Which pathway involves interactions between tissue factor (as cofactor), Factor VII, and Ca++?
Which factor deficiency leads to a serious bleeding tendency, although the intrinsic pathway is intact?
Which factor deficiency leads to a serious bleeding tendency, although the intrinsic pathway is intact?
What is the main process that dissolves & removes the fibrin clot following secondary hemostasis?
What is the main process that dissolves & removes the fibrin clot following secondary hemostasis?
What process occurs in distinct, but overlapping, steps known as Initiation, Amplification, and Propagation?
What process occurs in distinct, but overlapping, steps known as Initiation, Amplification, and Propagation?
What does the prothrombinase complex convert prothrombin (FII) to?
What does the prothrombinase complex convert prothrombin (FII) to?
Which of the following is involved in the primary complex formation with FVIIIa, Ca++, and phosphatidylserine in the Intrinsic Pathway?
Which of the following is involved in the primary complex formation with FVIIIa, Ca++, and phosphatidylserine in the Intrinsic Pathway?
Which of the following is released by endothelial cells to enhance antithrombin III (ATIII) & Tissue Factor Pathway Inhibitor (TFPI) activity in primary hemostasis?
Which of the following is released by endothelial cells to enhance antithrombin III (ATIII) & Tissue Factor Pathway Inhibitor (TFPI) activity in primary hemostasis?
What must be restricted to keep blood vessels patent during hemostasis?
What must be restricted to keep blood vessels patent during hemostasis?
Which physiological regulator acts as a physical barrier in global hemostasis?
Which physiological regulator acts as a physical barrier in global hemostasis?
Which factor is involved in the Extrinsic pathway and requires a cofactor to be activated?
Which factor is involved in the Extrinsic pathway and requires a cofactor to be activated?
In which pathway does the principal initiator of coagulation in vivo act?
In which pathway does the principal initiator of coagulation in vivo act?
Which physiological regulator is a cofactor for both Thrombin-activatable Carboxypeptidase B (TAFI) and activated protein C?
Which physiological regulator is a cofactor for both Thrombin-activatable Carboxypeptidase B (TAFI) and activated protein C?
Which factor deficiency leads to a serious bleeding tendency, although the extrinsic pathway is intact?
Which factor deficiency leads to a serious bleeding tendency, although the extrinsic pathway is intact?
What does the prothrombinase complex convert prothrombin (FII) to?
What does the prothrombinase complex convert prothrombin (FII) to?
What is the function of Polyphosphates released from dense granules in platelets during activation?
What is the function of Polyphosphates released from dense granules in platelets during activation?
What is the main initiator of coagulation in vivo?
What is the main initiator of coagulation in vivo?
Which factor forms a primary complex with high-molecular-weight kininogen (HMWK) & prekallikrein on collagen in the Intrinsic Pathway?
Which factor forms a primary complex with high-molecular-weight kininogen (HMWK) & prekallikrein on collagen in the Intrinsic Pathway?
Which of the following is true about the Common Pathway?
Which of the following is true about the Common Pathway?
Which pathway begins when blood comes into contact with collagen in damaged blood vessel wall?
Which pathway begins when blood comes into contact with collagen in damaged blood vessel wall?
What are the components involved in the Common Pathway?
What are the components involved in the Common Pathway?
Plasminogen activator inhibitor-1 is produced in the liver.
Plasminogen activator inhibitor-1 is produced in the liver.
Alpha2-Antiplasmin is produced in the liver.
Alpha2-Antiplasmin is produced in the liver.
Both intrinsic & extrinsic pathways activate the common pathway, resulting in production of fibrin to seal off the breach in blood vessel wall.
Both intrinsic & extrinsic pathways activate the common pathway, resulting in production of fibrin to seal off the breach in blood vessel wall.
What is the mechanism of action of Thrombin-activatable Carboxypeptidase B (TAFI)?
What is the mechanism of action of Thrombin-activatable Carboxypeptidase B (TAFI)?
What is the role of Alpha2-Antiplasmin in haemostasis?
What is the role of Alpha2-Antiplasmin in haemostasis?
What promotes plasminogen binding and activation by binding to lysine residues in fibrin?
What promotes plasminogen binding and activation by binding to lysine residues in fibrin?
Which physiological regulator is enhanced by heparin (exogenous) & heparin-like glycosaminoglycans (GAGs) on endothelial cells?
Which physiological regulator is enhanced by heparin (exogenous) & heparin-like glycosaminoglycans (GAGs) on endothelial cells?
The coagulation cascade is traditionally divided into 4 interacting pathways – intrinsic, extrinsic, common, and unique pathways. Which pathway involves interactions between tissue factor, Factor VII, and Ca++?
The coagulation cascade is traditionally divided into 4 interacting pathways – intrinsic, extrinsic, common, and unique pathways. Which pathway involves interactions between tissue factor, Factor VII, and Ca++?
Which factor deficiency leads to a serious bleeding tendency, although the intrinsic pathway is intact?
Which factor deficiency leads to a serious bleeding tendency, although the intrinsic pathway is intact?
What does the prothrombinase complex convert prothrombin (FII) to?
What does the prothrombinase complex convert prothrombin (FII) to?
Which physiological regulator inhibits the TF-FVIIa & TF-FVIIaFXa complexes?
Which physiological regulator inhibits the TF-FVIIa & TF-FVIIaFXa complexes?
What is the function of Polyphosphates released from dense granules in platelets during activation?
What is the function of Polyphosphates released from dense granules in platelets during activation?
What is true about the Intrinsic pathway?
What is true about the Intrinsic pathway?
What are the components of the Common Pathway in the coagulation cascade?
What are the components of the Common Pathway in the coagulation cascade?
What is the role of Alpha2-Antiplasmin in haemostasis?
What is the role of Alpha2-Antiplasmin in haemostasis?
Which physiological regulator is a cofactor for both Thrombin-activatable Carboxypeptidase B (TAFI) and activated protein C?
Which physiological regulator is a cofactor for both Thrombin-activatable Carboxypeptidase B (TAFI) and activated protein C?
What promotes plasminogen binding and activation by binding to lysine residues in fibrin?
What promotes plasminogen binding and activation by binding to lysine residues in fibrin?
In which pathway does the principal initiator of coagulation in vivo act?
In which pathway does the principal initiator of coagulation in vivo act?
What is true about the Intrinsic pathway?
What is true about the Intrinsic pathway?
What is the role of thrombin-activatable carboxypeptidase B (TAFI) in the haemostasis process?
What is the role of thrombin-activatable carboxypeptidase B (TAFI) in the haemostasis process?
How does protein C contribute to haemostasis?
How does protein C contribute to haemostasis?
What is the mechanism of action of alpha2-antiplasmin in haemostasis?
What is the mechanism of action of alpha2-antiplasmin in haemostasis?
What is the function of plasminogen activator inhibitor-1 (PAI-1) in fibrinolysis?
What is the function of plasminogen activator inhibitor-1 (PAI-1) in fibrinolysis?
How does thrombin-activatable carboxypeptidase B (TAFI) promote fibrinolysis?
How does thrombin-activatable carboxypeptidase B (TAFI) promote fibrinolysis?
What is the role of extracellular nuclear material in the context of haemostasis?
What is the role of extracellular nuclear material in the context of haemostasis?
What is the main process that dissolves and removes the fibrin clot following secondary haemostasis?
What is the main process that dissolves and removes the fibrin clot following secondary haemostasis?
What is the principal initiator of coagulation in vivo?
What is the principal initiator of coagulation in vivo?
What physiological regulator acts as a physical barrier in global haemostasis?
What physiological regulator acts as a physical barrier in global haemostasis?
What process occurs in distinct, but overlapping, steps known as Initiation, Amplification, and Propagation?
What process occurs in distinct, but overlapping, steps known as Initiation, Amplification, and Propagation?
What is the principal initiator of coagulation in vivo?
What is the principal initiator of coagulation in vivo?
What is the alternate name for the TF-FVIIa complex in the extrinsic pathway?
What is the alternate name for the TF-FVIIa complex in the extrinsic pathway?
Which factor forms a primary complex with high-molecular-weight kininogen (HMWK) & prekallikrein on collagen in the Intrinsic Pathway?
Which factor forms a primary complex with high-molecular-weight kininogen (HMWK) & prekallikrein on collagen in the Intrinsic Pathway?
What is the role of Factor IX (FIX) in the Common Pathway?
What is the role of Factor IX (FIX) in the Common Pathway?
What is the function of the prothrombinase complex?
What is the function of the prothrombinase complex?
What are the distinct, overlapping steps of secondary haemostasis in the modern cell-based model?
What are the distinct, overlapping steps of secondary haemostasis in the modern cell-based model?
What is the main enzyme that mediates fibrinolysis?
What is the main enzyme that mediates fibrinolysis?
What is the role of plasminogen activators in fibrinolysis?
What is the role of plasminogen activators in fibrinolysis?
How is the size of the primary and secondary haemostatic plugs restricted to keep blood vessels patent?
How is the size of the primary and secondary haemostatic plugs restricted to keep blood vessels patent?
What is the mechanism of action of thrombomodulin in secondary haemostasis?
What is the mechanism of action of thrombomodulin in secondary haemostasis?
Which two cell types are required for the process of secondary haemostasis as proposed by the modern cell-based model?
Which two cell types are required for the process of secondary haemostasis as proposed by the modern cell-based model?
What is the function of Alpha2-Antiplasmin in haemostasis?
What is the function of Alpha2-Antiplasmin in haemostasis?
