Thrombis meduim Quiz

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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