Questions and Answers
What role does von Willebrand factor (vWF) play in platelet adhesion?
Which substance primarily triggers platelet aggregation in addition to ADP?
What initiates the synthesis of tissue factor in endothelial cells?
What is the result of thrombin binding to platelet surface receptors?
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What is the significance of the 'viscous metamorphosis' in hemostasis?
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What type of granules release contents immediately after platelet adhesion?
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What is the primary enzyme responsible for fibrinolysis?
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Which pathway produces plasmin from plasminogen?
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Which of the following is NOT a component of Virchow's triad influencing thrombus formation?
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What type of disorder is Antithrombin III deficiency classified as?
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How does turbulence in blood flow contribute to thrombus formation?
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Which condition is considered a secondary cause of hypercoagulability?
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In which part of the cardiovascular system can thrombi develop?
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What can cause endothelial injury, one of the factors influencing thrombus formation?
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Which venous thrombi are most likely to embolize?
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What is a common cause of cardiac mural thrombi?
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What percentage of emboli represent dislodged thrombi?
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What condition can lead to atrial mural thrombi?
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Which of the following is NOT a consequence of thromboembolism?
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What is the incidence rate of pulmonary embolism among hospitalized patients?
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What is the direction of growth for arterial thrombi?
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What characteristics distinguish venous thrombi from arterial thrombi?
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What are the lines of Zahn?
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Which type of thrombus is formed primarily through platelet activation?
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Which process describes the fate of a thrombus that leads to its dissolution?
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What potential clinical danger does venous thrombus pose?
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What is the primary role of platelets in venous thrombosis?
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What is a mural thrombus?
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What is the outcome of arterial thrombi in critical vascular sites?
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How do arterial thrombi typically appear in terms of structure?
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Study Notes
Fibrinolytic and Prothrombotic Properties
- Plasminogen activator (t-PA) is crucial in the conversion of plasminogen to plasmin for clot dissolution.
- Endothelial injury promotes platelet adhesion via von Willebrand factor (vWF), establishing a connection with collagen.
- Endothelial cells produce tissue factor upon activation by bacterial endotoxin or cytokines (e.g., TNF, IL-1), initiating the extrinsic clotting cascade.
- Endothelial cells release inhibitors of plasminogen activator (PAIs), impeding fibrinolysis.
Role of Platelets
- Central players in hemostasis: mediating adhesion, secretion, aggregation, and clot formation.
- Platelet adhesion occurs through vWF bridging platelet receptors (e.g., GpIb) with collagen.
- Upon adhesion, platelets release dense granule contents, including ADP, calcium, and serotonin, leading to platelet activation.
- Thromboxane A2 (TXA2) and ADP are essential for platelet aggregation, forming a temporary hemostatic plug.
- Thrombin activation enhances platelet aggregation, resulting in a stable secondary hemostatic plug through irreversible fusion.
Thrombosis Pathogenesis
- Virchow's triad includes endothelial injury, blood flow abnormalities (stasis or turbulence), and hypercoagulability, influencing thrombus formation.
- Endothelial injury can occur without physical disruption, altering the balance of prothrombotic and antithrombotic signals.
Alterations in Blood Flow
- Turbulent blood flow can lead to both arterial and cardiac thrombosis by causing endothelial injury and forming stasis pockets, particularly affecting venous thrombus development.
Hypercoagulability
- Hypercoagulability can be primary (genetic mutations) or secondary (acquired conditions).
- Primary examples include factor V Leiden mutation, prothrombin gene mutation, and antithrombin III deficiency.
- Secondary causes include prolonged immobility, myocardial infarction, atrial fibrillation, cancer, and tissue injury.
Thrombus Morphology
- Thrombi can form throughout the cardiovascular system, with size and shape influenced by location and cause.
- Arterial thrombi often grow retrograde from attachment, while venous thrombi extend along blood flow.
- Thrombi may exhibit lines of Zahn and are classified as mural or occlusive, with venous thrombi usually being occlusive.
Fate of Thrombus
- Thrombi can propagate, embolize, dissolve, or undergo organization and recanalization.
Clinical Correlations: Venous vs. Arterial Thrombosis
- Venous thrombi pose risks for congestion, edema, and pulmonary embolism, while arterial thrombi significantly impact critical vascular sites, leading to tissue infarction.
- Superficial venous thrombi typically do not embolize, but deep vein thrombi (e.g., femoral) pose serious risks for embolization.
Cardiac and Arterial Thrombosis
- Atherosclerosis contributes to thrombus formation via endothelial damage and abnormal circulation.
- Cardiac mural thrombi can arise following myocardial infarction or rheumatic heart disease associated with atrial dilation and fibrillation.
Embolism
- An embolus is a detached intravascular mass that can lead to ischemic tissue damage or infarction.
- Most emboli are thromboembolic in nature, with other rare types including fat droplets and air bubbles.
Pulmonary Thromboembolism
- Incidence rate is 20 to 25 per 100,000 hospitalized patients, accounting for approximately 200,000 U.S. deaths annually.
- 95% of pulmonary emboli originate from deep leg vein thrombi.
- Sudden death may occur if over 60% of pulmonary circulation is obstructed.
Systemic Thromboembolism
- Predominantly arises from mural thrombi associated with infarcts and dilated left atria.
- Common destinations include lower extremities (75%) and the brain (10%).
Deep Vein Thrombosis (DVT)
- Predisposing factors include immobility, pregnancy, surgery, severe burns, and heart failure.
- High-risk patients require preventive measures, including heparin and leg compression during surgery.
- Treatment typically involves intravenous heparin and warfarin.
Fat Embolism
- Can occur after long bone fractures or soft-tissue trauma, leading to pulmonary insufficiency and neurologic symptoms.
- Fatality in approximately 10% of fat embolism syndrome cases, with signs including anemia and thrombocytopenia.
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