Thrombosis : Definition, Causes, Types, Morphology, Fate of a Thrombus & Clinical manifestations

Summary

This video provides a comprehensive overview of thrombosis, explaining its causes, types, and clinical manifestations. It covers Virchow’s triad, which includes endothelial injury, alterations in blood flow, and hypercoagulability, as key contributors to thrombus formation. The video discusses the different types of thrombi—arterial, venous, mural, and vegetative—along with their pathophysiology and outcomes such as embolization, propagation, or resolution. Clinical manifestations, including ischemia, infarction, and pulmonary embolism, are also highlighted. Additionally, the differences between ante-mortem and post-mortem clots are clarified, providing a detailed and accessible guide to understanding thrombosis.

Takeaways

• 😀 Thrombosis is the formation of a structured, solid blood clot within the vascular system, unlike post-mortem clotting or hematoma formation.
• 😀 The body has natural mechanisms to prevent thrombosis, including anti-platelet, anticoagulant, and fibrinolytic effects produced by endothelial cells.
• 😀 Endothelial cells secrete nitric oxide and prostacyclin to prevent platelet aggregation, and they also produce adenosine diphosphatase to further inhibit platelet activation.
• 😀 Coagulation is controlled by factors like heparin-like molecules and thrombomodulin, which inhibit clotting pathways, preventing unnecessary clot formation.
• 😀 Virchow's triad identifies three main factors that contribute to thrombosis: endothelial injury, abnormal blood flow (turbulence or stasis), and hypercoagulability.
• 😀 Endothelial injury often results from causes such as atherosclerosis, hypertension, vasculitis, and hypoxia, leading to platelet adhesion and thrombosis.
• 😀 Abnormal blood flow can occur from turbulence (common in arteries) or stasis (common in veins), both of which can promote thrombosis.
• 😀 Hypercoagulability is less common but still a significant cause, involving genetic mutations or acquired factors like immobilization or surgery.
• 😀 Arterial thrombi typically form in response to endothelial injury and turbulence, while venous thrombi are primarily caused by stasis of blood flow.
• 😀 Thrombosis can lead to serious complications like ischemia, infarction, and embolism, with the potential to cause myocardial infarction, stroke, or pulmonary embolism.

Q & A

What is thrombosis and how is it different from post-mortem clotting?

Thrombosis is the formation of blood clots within the vascular system due to activation of hemostatic mechanisms while the person is alive. Post-mortem clotting occurs after death and is not caused by hemostatic mechanisms; it forms differently and does not involve the platelets and fibrin characteristic of thrombosis.

What role do endothelial cells play in preventing thrombosis?

Endothelial cells prevent thrombosis by producing factors that block platelet adhesion and aggregation, inhibit coagulation, and lyse clots. These effects include anti-platelet, anticoagulant, and fibrinolytic actions, which help maintain normal blood flow and prevent clot formation.

What are the three primary factors of Virchow's triad that contribute to thrombosis?

Virchow's triad includes endothelial injury, alterations in normal blood flow (turbulence or stasis), and hypercoagulability of blood. These factors can individually or synergistically promote thrombosis.

How does endothelial injury lead to thrombosis?

Endothelial injury exposes the sub-endothelium, allowing platelets to adhere and aggregate. This initiates the coagulation cascade, leading to fibrin deposition and the formation of a thrombus. Dysfunctional endothelial cells also increase pro-coagulant factors, further promoting thrombosis.

What is the difference between turbulence and stasis in blood flow and how do they contribute to thrombosis?

Turbulence disrupts laminar blood flow, bringing platelets into contact with the endothelium, causing endothelial injury and promoting thrombosis. Stasis, where blood flow is stagnant, particularly contributes to venous thrombi by enhancing pro-coagulant activity and preventing the dilution of clotting factors.

How does hypercoagulability contribute to thrombosis?

Hypercoagulability is a condition where the coagulation pathways are altered, making the blood more prone to clotting. This can be genetic (e.g., factor V Leiden mutation) or acquired (e.g., prolonged bed rest, cancer, or surgery), and increases the risk of thrombosis.

What are the characteristic features of arterial thrombi?

Arterial thrombi are typically non-occlusive in large vessels but may be occlusive in small vessels. They are composed of alternating bands of platelets and fibrin (lines of Zonn), with darker areas representing red blood cells. They commonly cause ischemia and infarction in tissues supplied by the affected artery.

What are the differences between thrombophlebitis and phlebothrombosis?

Thrombophlebitis involves inflammation of veins, leading to thrombosis, and the thrombus is attached to the vessel wall. Phlebothrombosis, on the other hand, is characterized by venous thrombosis without inflammation, and stasis plays a major role in its formation.

How do venous thrombi differ from arterial thrombi in appearance and composition?

Venous thrombi are typically more red in color, consisting mostly of red blood cells and fewer platelets. In contrast, arterial thrombi have more platelets and fibrin, leading to alternating pale and dark bands known as lines of Zonn.

What is the fate of a thrombus, and what are the possible outcomes after its formation?

The fate of a thrombus can involve propagation, embolization, dissolution, organization, or recanalization. Propagation leads to an increase in thrombus size, embolization occurs when the thrombus dislodges and travels to other sites, and dissolution is the breakdown of thrombi by fibrinolysis. Older thrombi may undergo organization or recanalization to restore some blood flow through the affected vessel.