Deep vein thrombosis
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Deep vein thrombosis
Cardiovascular system
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Cardiovascular system pathology review
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
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Cardiomyopathies: Pathology review
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Deep vein thrombosis
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Reproduced from: Radiopaedia
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Deep venous thrombosis (DVT) p. 697
direct factor Xa inhibitors for p. 445
embolic stroke and p. 529
glucagonomas and p. 357
heparin for p. 443
labs/findings p. 721
tamoxifen/raloxifen and p. 449
Enoxaparin p. 443
deep venous thrombosis p. 696
Heparin p. 443
deep venous thrombosis p. 696
Pulmonary embolism p. 697
deep venous thrombosis and p. 697
Rivaroxaban p. 444
deep venous thrombosis p. 696
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Transcript
Content Reviewers
Rishi Desai, MD, MPH“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.
Sources
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
- "Deep vein thrombosis and pulmonary embolism" The Lancet (2016)
- "Deep vein thrombosis" Hematology (2014)
- "Diagnosis of deep-vein thrombosis" Thrombosis Research (2018)
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