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PH-FD05

Thrombosis and embolism

Why blood that should stay fluid clots inside a vessel, why arterial and venous thrombi differ, and where a fragment that breaks free travels and lodges.

By the end, you can

  • Describe how the endothelium keeps blood fluid and how platelets and fibrin form a clot when a vessel is injured.
  • Use Virchow’s triad to explain why thrombi form inside intact circulation.
  • Compare arterial and venous thrombi in their causes, composition and consequences.
  • Trace where emboli from the leg veins, the left heart and the carotid arteries lodge.
  • Describe the possible fates of a thrombus and the effects on the tissue beyond it.
  • Recognise the classic appearances, types of embolus and tests examiners ask about, and explain how antiplatelet, anticoagulant and fibrinolytic drugs act on the mechanism.

What it is

Thrombosis is the formation of a solid mass of platelets, fibrin and trapped blood cells (a thrombus) inside a vessel or the heart during life. An embolus is any mass carried in the blood to lodge elsewhere; most are fragments of thrombus (thromboembolism), but fat, air, amniotic fluid and plaque contents can also embolise.

3 types to tell apart
Arterial thrombosis
Forms in fast flow on a damaged wall, usually a ruptured atherosclerotic plaque; rich in platelets; blocks supply and causes ischaemia.
Venous thrombosis
Forms in slow flow, often in the valve pockets of deep leg veins; rich in fibrin and red cells; blocks drainage and can embolise to the lungs.
Cardiac (mural) thrombosis
Forms in a chamber where blood stagnates, such as the left atrial appendage in atrial fibrillation or over an infarct; emboli enter the systemic arteries.

Normal function

Blood stays fluid until a vessel is cut

Healthy endothelium lines the and actively prevents clotting: it releases nitric oxide and prostacyclin, which keep platelets inactive, carries molecules (thrombomodulin, heparan sulfate) that switch on natural anticoagulants, and releases tissue plasminogen activator, which starts the breakdown of fibrin.

When a vessel is cut, collagen and von Willebrand factor beneath the endothelium are exposed. Platelets stick to them, become activated, release ADP and thromboxane A2, and bind to one another through fibrinogen: a platelet plug. Tissue factor from the damaged wall starts the coagulation cascade, which makes thrombin; thrombin converts fibrinogen into a mesh of fibrin that binds the plug.

Antithrombin, proteins C and S and the fibrinolytic system keep the clot small and local. Thrombosis is this normal process switched on in the wrong place.

Point to it on the model