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Bundle branch block
Pulseless electrical activity
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature atrial contraction
Long QT syndrome and Torsade de pointes
Premature ventricular contraction
Coronary steal syndrome
Coarctation of the aorta
Polycystic kidney disease
Renal artery stenosis
Peripheral artery disease
Subclavian steal syndrome
Superior mesenteric artery syndrome
Human herpesvirus 8 (Kaposi sarcoma)
Chronic venous insufficiency
Deep vein thrombosis
Acyanotic congenital heart defects: Pathology review
Aortic dissections and aneurysms: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Cardiac and vascular tumors: Pathology review
Cardiomyopathies: Pathology review
Coronary artery disease: Pathology review
Cyanotic congenital heart defects: Pathology review
Dyslipidemias: Pathology review
Endocarditis: Pathology review
Heart blocks: Pathology review
Heart failure: Pathology review
Hypertension: Pathology review
Pericardial disease: Pathology review
Peripheral artery disease: Pathology review
Shock: Pathology review
Supraventricular arrhythmias: Pathology review
Valvular heart disease: Pathology review
Vasculitis: Pathology review
Ventricular arrhythmias: Pathology review
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pancreatic cancer p. 406
vancomycin p. 187
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.
Thrombophlebitis is a blood clot that gets lodged in a vein and causes inflammation. All factors that lead to abnormal clot formation are grouped into three factors, known as Virchow's triad. They include venous stasis; a state of hypercoagulation; and damage to the endothelial cell lining. Venous stasis is said when blood doesn't flow appropriately in the veins, which can occur in situations of prolonged periods of inactivity. Endothelial injury can occur when there is an injury or trauma to a blood vessel; and finally, hypercoagulable states can be seen in certain conditions like cancer, pregnancy, and certain medications such as hormonal birth control or chemotherapy.
Thrombophlebitis can cause pain, swelling, and redness in the affected area, and may be accompanied by a fever. In some cases, a clot can break loose from the vein and travel to the lungs, causing a pulmonary embolism, which can be life-threatening. The treatment of thrombophlebitis involves thrombolytics to help break down the clot, or a thrombectomy, which is an intervention that aims to surgically remove the clot. Long-term treatment to prevent future thrombi from forming can include anticoagulant medications like warfarin or heparin.
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