Thrombophlebitis

Thrombophlebitis can be broken down into “thrombo” or thrombus which refers to a blood clot, “phleb” which refers to a vein, and “itis” which refers to inflammation. So thrombophlebitis is a blood clot that gets lodged in a vein and causes inflammation.

Normally, the process starts with damage to the endothelium, or inner lining of the blood vessel walls, after which there’s an immediate vasoconstriction or narrowing of the blood vessel which limits the amount of blood flow. After that, some platelets adhere to the damaged vessel wall, and become activated by collagen and tissue factor, which are proteins that are normally kept separated from the blood by an intact endothelium. These platelets then recruit additional platelets to form a platelet plug. The formation of the platelet plug is called primary hemostasis.

After that, the coagulation cascade is activated. First off in the blood there’s a set of clotting factors, most of which are proteins synthesized by the liver, and usually these are inactive and just floating around in the blood. The coagulation cascade starts when one of these proteins gets proteolytically cleaved. This active protein then proteolytically cleaves and activates the next clotting factor, and so on. The final step is activation of the protein fibrinogen to fibrin, which deposits and polymerizes to form a mesh around the platelets. So these steps leading up to fibrin reinforcement of the platelet plug make up the process called secondary hemostasis and results in a hard clot at the site of the injury.

This cascade has a huge degree of amplification and takes only a few minutes from injury to clot formation. So the activation of the cascade is carefully controlled by anticoagulation proteins that target and inactivate key clotting factors. For example, antithrombin inactivates Factors IXa, Xa, XIa, XIIa, VIIa and thrombin while protein C inactivates Factors Va and VIIIa.

As the clot grows in size, it limits the amount of blood able to pass by, and pressure in the vein increases. Usually the clot might start naturally breaking down, for example, enzymes like plasmin break down fibrin into fragments called D-dimers.