Cardiovascular Pathologies: Thrombosis and Embolism

Question-and-answer flashcards covering definitions, mechanisms, risk factors, and clinical consequences of thrombosis, embolism, DVT, and pulmonary embolism.

What is a thrombus?

A clotted mass of blood that forms within the cardiovascular system during life.

What is an embolus?

An intravascular solid, liquid, or gaseous mass that is carried by the bloodstream to a site remote from its origin or point of entry.

Which type of embolus is most common?

Thrombo-embolus (a detached fragment of a thrombus).

Name four major categories of emboli.

Thrombo-emboli, athero-emboli, septic emboli, and fat emboli.

Outline the main biochemical steps of normal haemostasis.

Platelet activation → platelet plug → prothrombin is converted to thrombin → thrombin converts fibrinogen to fibrin, stabilising the clot.

Which enzyme is chiefly responsible for breaking down cross-linked fibrin during fibrinolysis?

Plasmin.

State the three components of Virchow’s triad that promote thrombus formation.

Endothelial injury, abnormal blood flow, and hypercoagulability.

Give three causes of endothelial injury.

Atherosclerosis, mechanical damage (e.g., catheter), infection, radiation, or scar tissue replacing myocardium post-infarct (any three).

How does healthy endothelium normally prevent coagulation?

It expresses platelet inhibitors and anticoagulant proteins (e.g., anti-thrombin, tissue factor pathway inhibitor, protein C pathway) that suppress platelet adhesion and the coagulation cascade.

Name two key procoagulant factors that damaged endothelium begins to express.

Tissue factor and von Willebrand factor (also adhesion molecules).

What is laminar blood flow?

A flow pattern in which the velocity is highest in the centre of the vessel and lowest near the endothelium, minimising interaction between blood components and the vessel wall.

Why does disruption of laminar flow favour thrombosis?

It brings platelets and clotting factors into contact with the endothelium, especially if the endothelium is already damaged or activated.

Identify the two principal forms of abnormal blood flow.

Turbulence and stasis.

List four conditions that can create turbulence or stasis leading to thrombosis.

Atherosclerotic plaques, aneurysms, myocardial infarction (non-contractile myocardium), and prolonged immobility causing venous stasis.

Differentiate primary from secondary hypercoagulable states with an example of each.

Primary = inherited clotting disorder (e.g., Factor V Leiden); Secondary = acquired risk (e.g., cancer, smoking, obesity, pregnancy, major surgery).

Name the four possible fates of a thrombus if the patient survives the initial event.

Propagation, embolization, dissolution, and organisation with recanalization (scarring).

Where do arterial or cardiac thrombi usually start and in which direction do they grow?

They begin at sites of endothelial injury or turbulence and grow retrograde (against blood flow).

Where do venous thrombi most commonly form and how do they propagate?

They form at sites of stasis in the deep veins of the lower extremities and extend in the direction of blood flow toward the heart; the propagating portion is often loosely attached.

Why do venous thrombi contain more red blood cells than arterial thrombi?

Because they form in slower venous circulation, allowing more RBCs to become enmeshed within the fibrin mesh.

Why are deep-vein thrombi (DVT) more clinically significant than superficial vein thrombi?

Deep veins are surrounded by muscle; muscle contractions can dislodge the clot, allowing it to travel to the lungs and cause a pulmonary embolism.

Explain how venous stasis promotes DVT formation.

Venous stasis promotes DVT formation through several mechanisms: it reduces the normal shear stress on the endothelium, leading to endothelial dysfunction where the cells lose their anticoagulant properties and may express procoagulant factors; it prevents dilution of activated clotting factors, allowing them to accumulate and initiate the coagulation cascade; and it physically allows platelets, fibrin, and red blood cells to aggregate more readily due to the lack of dispersion by rapid blood flow, ultimately forming a thrombus.

Provide one example each from the three risk-factor categories for DVT (hypercoagulability, vessel wall injury, alterations in blood flow).

Hypercoagulability – postoperative state; Vessel wall injury – trauma or smoking; Altered flow – prolonged immobilisation.

Are most DVTs symptomatic or asymptomatic?

Most are asymptomatic.

Trace the path a thrombus from a leg DVT takes to reach the lungs.

Deep vein → inferior vena cava → right atrium → right ventricle → pulmonary artery → smaller pulmonary arteries where it may lodge.

What happens when a pulmonary embolus lodges in a small branch of the pulmonary artery?

It blocks blood flow, preventing oxygenation of blood; if large enough, it can impede right-ventricular outflow and reduce left-ventricular preload.

Why are pulmonary infarcts relatively uncommon after embolism?

The lungs have dual (collateral) circulation from both the bronchial and pulmonary arteries.

Obstruction of approximately what percentage of the pulmonary circulation can cause sudden death?

About 60 % obstruction can produce sudden death due to acute right-heart failure and circulatory collapse.

Where do most systemic arterial emboli originate?

From the heart (≈ 80 %), predominantly from left-ventricular wall infarcts or left-atrial dilation/fibrillation.

Which two destinations receive the majority of systemic arterial emboli?

The lower extremities (≈ 75 %) and the brain (≈ 10 %).

List three factors that determine the clinical consequences of a systemic embolus.

Tissue vulnerability to ischaemia, calibre of the occluded vessel, and the presence or absence of collateral blood supply.