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direct factor Xa inhibitors for p. 442
embolic stroke and p. 525
glucagonomas and p. 355
heparin for p. 440
labs/findings p. 727
tamoxifen/raloxifen and p. 445
deep venous thrombosis p. 690
deep venous thrombosis p. 690
deep venous thrombosis and p. 691
deep venous thrombosis p. 690
“Deep vein” refers to the veins that typically run between muscles as they travel back towards the heart, as opposed to superficial veins that you can see on the surface, and “thrombosis” refers to a blood clot. So a deep vein thrombosis or DVT is a blood clot in one of those deep veins.
Normally, blood makes it back to the heart from the tissues and organs via a network of veins that merge over and over. Superficial veins drain blood into deep veins, which rely on the skeletal muscle pump to move blood forward. The way it works is that the surrounding skeletal muscles compress the vein and propel blood forward, and the veins prevent blood from moving backwards by using one-way valves.
Ultimately, all of the blood ends up in the superior or inferior vena cava and then dumps into the right atrium. From there, the blood goes into the right ventricle and before being pumped into the pulmonary artery and eventually into the lungs. Deep vein thrombosis most commonly develops in the lower legs, below the knee, although blood clots can form in both superficial and deep veins and in other parts of the body as well.
Normally, the process starts with damage to the endothelium or inner lining of blood vessel walls, after which there’s an immediate vasoconstriction or narrowing of the blood vessel, limiting the amount of blood flow. After that, some platelets adhere to the damaged vessel wall, and become activated by collagen and tissue factor, proteins that are normally kept separate from the blood by the intact endothelium. These platelets then recruit additional platelets, forming a 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; usually these are inactive and just float around in the blood. The coagulation cascade starts when one of these proteins gets proteolytically cleaved. This active protein begins a chain reaction, proteolytically cleaving 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. These steps leading up to fibrin reinforcement of the platelet plug make up the process called secondary hemostasis; this results in a hard clot at the site of the injury.
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