Cardiovascular - Deep Vein Thrombosis Midterm Notes PDF
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University of Windsor
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Summary
This document provides a detailed overview of deep vein thrombosis (DVT), covering its causes, pathophysiology, transmission, and various risk factors. It explores the roles of venous stasis, endothelial injury, and hypercoagulability. This is study material, suitable for undergraduate medical students.
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3 1 CARDIOVASCULAR – Deep Vein Thrombosis 1. Most Likely Cause Cause: o The primary cause of DVT is the development of blood clots in the deep veins, most commonly in the...
3 1 CARDIOVASCULAR – Deep Vein Thrombosis 1. Most Likely Cause Cause: o The primary cause of DVT is the development of blood clots in the deep veins, most commonly in the lower extremi;es. o The main factors promo;ng DVT are described by Virchow's Triad, which includes: § Venous stasis: Reduced blood flow due to immobility, long flights, prolonged bed rest, heart failure, or obesity. § Endothelial injury: Damage to the inner lining of veins caused by surgery, trauma, or medica;ons. § Hypercoagulability: Increased tendency of blood to clot due to factors such as gene;c muta;ons (e.g., Factor V Leiden), pregnancy, oral contracep;ve use, or cancer. 2. Pathophysiology Mechanism of Disease Development: o Venous Stasis: Prolonged immobility reduces blood flow, allowing blood to pool in the lower extremi;es. o Endothelial Damage: Injury to the endothelium triggers the release of pro- coagulant factors and the recruitment of platelets to the site of injury. o Hypercoagulability: Condi;ons like Factor V Leiden muta;on, Protein C/S deficiency, pregnancy, or the use of oral contracep;ves increase blood clot forma;on. o Thrombus FormaLon: § Platelets adhere to the endothelium, become ac;vated, and release thromboxane A2, which promotes further platelet aggrega;on. § The coagulaLon cascade is ac;vated, leading to the conversion of fibrinogen to fibrin, stabilizing the clot. § Clot PropagaLon: The clot can grow in size and poten;ally become dislodged, leading to pulmonary embolism (PE) if it travels to the lungs. 3. Disease Transmission Transmission: o Not transmissible. DVT is a non-communicable disease that arises from lifestyle, geneLc, and physiological factors. o There is no direct transmission of DVT from one person to another. 4. Risk Factors Modifiable Risk Factors: o Immobility: Prolonged bed rest, long-haul flights, or siLng for long periods. o Surgery and Trauma: Damage to veins during orthopedic or abdominal surgery increases clot risk. 2 o Obesity: Excess weight increases venous pressure, leading to venous stasis. o MedicaLons: Use of oral contracepLves or hormone replacement therapy (HRT) increases cloLng risk due to estrogen's effect on cloLng factors. o Pregnancy: During pregnancy, hormonal changes and increased abdominal pressure can reduce venous return, promo;ng stasis. o Cancer: Certain cancers can increase the produc;on of pro-coagulant factors, promo;ng clot forma;on. Non-Modifiable Risk Factors: o Age: Older adults are at greater risk due to reduced mobility and venous insufficiency. o GeneLcs: Inherited thrombophilias such as Factor V Leiden mutaLon, Protein C or Protein S deficiency, and AnLthrombin III deficiency increase the risk of DVT. o Medical CondiLons: Heart failure, stroke, and paralysis are associated with reduced mobility and venous stasis. Summary Table Criteria Deep Vein Thrombosis (DVT) Most Likely Blood clot forma;on in deep veins due to Venous stasis, Endothelial injury, Cause and Hypercoagulability (Virchow's Triad). 1. Stasis: Blood pools in veins. 2. Endothelial damage: Ac;vates platelets. 3. Pathophysiology Hypercoagulability: Increased cloLng tendency leads to fibrin clot forma;on. Transmission Not transmissible. Caused by lifestyle, gene;c, and physiological factors. Modifiable: Prolonged immobility, surgery, obesity, medica;ons, cancer, Risk Factors pregnancy. Non-Modifiable: Age, gene;cs (Factor V Leiden, Protein C/S deficiency), heart failure.