Thrombis meduim Quiz

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Questions and Answers

What role does von Willebrand factor (vWF) play in platelet adhesion?

It activates the intrinsic clotting cascade.

It inhibits platelet aggregation.

It acts as a bridge between platelet receptors and collagen. (correct)

It stimulates the release of thrombin.

Which substance primarily triggers platelet aggregation in addition to ADP?

Epinephrine

Thromboxane A2 (TXA2) (correct)

Serotonin

Histamine

What initiates the synthesis of tissue factor in endothelial cells?

Oxidative stress

Bacterial endotoxins or cytokines (correct)

Low levels of oxygen

Increased shear stress

What is the result of thrombin binding to platelet surface receptors?

Further platelet aggregation and contraction Signup and view all the answers

What is the significance of the 'viscous metamorphosis' in hemostasis?

It marks the transition to an irreversible hemostatic plug. Signup and view all the answers

What type of granules release contents immediately after platelet adhesion?

Both alpha and dense body granules Signup and view all the answers

What is the primary enzyme responsible for fibrinolysis?

Plasmin Signup and view all the answers

Which pathway produces plasmin from plasminogen?

Factor XII-dependent pathway Signup and view all the answers

Which of the following is NOT a component of Virchow's triad influencing thrombus formation?

Increased platelet count Signup and view all the answers

What type of disorder is Antithrombin III deficiency classified as?

Primary disorder Signup and view all the answers

How does turbulence in blood flow contribute to thrombus formation?

It creates pockets of stasis Signup and view all the answers

Which condition is considered a secondary cause of hypercoagulability?

Prolonged bedrest Signup and view all the answers

In which part of the cardiovascular system can thrombi develop?

In cardiac chambers, valves, arteries, and veins Signup and view all the answers

What can cause endothelial injury, one of the factors influencing thrombus formation?

Turbulent blood flow Signup and view all the answers

Which venous thrombi are most likely to embolize?

Deep venous thrombi above the knee Signup and view all the answers

What is a common cause of cardiac mural thrombi?

Myocardial infarction Signup and view all the answers

What percentage of emboli represent dislodged thrombi?

99% Signup and view all the answers

What condition can lead to atrial mural thrombi?

Mitral valve stenosis Signup and view all the answers

Which of the following is NOT a consequence of thromboembolism?

Increased blood flow Signup and view all the answers

What is the incidence rate of pulmonary embolism among hospitalized patients?

20 to 25 per 100,000 Signup and view all the answers

What is the direction of growth for arterial thrombi?

Retrograde from the point of attachment Signup and view all the answers

What characteristics distinguish venous thrombi from arterial thrombi?

Appear red and often occlude blood flow Signup and view all the answers

What are the lines of Zahn?

Gross and microscopic laminations in thrombi Signup and view all the answers

Which type of thrombus is formed primarily through platelet activation?

Arterial thrombus Signup and view all the answers

Which process describes the fate of a thrombus that leads to its dissolution?

Dissolution Signup and view all the answers

What potential clinical danger does venous thrombus pose?

Leading to pulmonary embolism Signup and view all the answers

What is the primary role of platelets in venous thrombosis?

They play a secondary role compared to coagulation activation Signup and view all the answers

What is a mural thrombus?

A thrombus in heart chambers or the aortic lumen Signup and view all the answers

What is the outcome of arterial thrombi in critical vascular sites?

They can lead to downstream tissue infarction Signup and view all the answers

How do arterial thrombi typically appear in terms of structure?

A friable meshwork of components Signup and view all the answers

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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