Venous disease Flashcards
What is varicose veins? What causes it?
Varicose veins are dilated superficial vessels that develop in the lower extremities. Varicosity results from intrinsic weakness of the vessel wall, from increased intraluminal pressure or from defects in the structure and function of venous valves.
Primary varicose veins VS secondary varicose viens
Primary varicose veins originate in the superficial system, and factors that lead to their development include pregnancy, prolonged standing, and obesity (adipose tissue surrounding vessel walls offers less structural support to veins than does lean mass).
Secondary varicose veins occur when an abnormality (deep venous insufficiency or occlusion) in the deep venous system is the cause of superficial varicosities. In this case, deep venous blood is hunted retrograde through perforating channels into superficial veins, increasing intraluminal pressure and volume and causing dilation and varicosity formation.
Superficial venous insufficiency may result when venous valves are unable to function normally in the dilated veins. This causes swelling and skin ulceration that is particularly severe near the ankle.
How are varicose veins treated?
Varicose veins are treated with sclerotherapy, thermal ablation, or surgery. Sclerotherapy involves the localized intravenous administration of an irritating chemical agent to fibrose varicose veins. Endovenous thermal ablation procedures use laser or radiofrequency catheters to deliver heat energy, which induces thromboses and is used to obliterate varicose great saphenous veins. Surgical therapy involves direct vein ligation and removal.
What is chronic venous insufficiency? How does it occur?
It is characterized by elevated venous pressure with extravasation of edema into the tissue of the lower extremities. CVI develops when venous blood return to the heart is impaired by mechanisms that include valvular incompetence of deep or superficial veins, venous obstruction, and calf muscle pump dysfunction. A secondary form of CVI is postphlebitic syndrome, resulting from venous valvular damage or persistent venous occlusion after deep vein thrombosis.
What are the symptoms of chronic venous insufficiency?
Pain or achiness in the legs, particular when standing for prolonged periods.
What are the physical finding of venous thromboembolism?
inflammatory response in the vessel wall that it incites. Initially, the venous thrombus is composed of platelets and fibrin. Later, red blood cells become interspersed within the fibrin, and the thrombus tends to propagate in the direction of blood flow. The changes in the vessel wall can be minimal or can include granulocyte infiltration, loss of endothelium and edema.
What is venous thromboembolsim? what does the emboli contain at its early stage and what does it contain at it late stages?
Venous thrombosis is thrombus formation within a superficial or deep vein and the inflammatory response in the vessel wall that it incites. Initially, the venous thrombus is composed of platelets and fibrin. Later, red blood cells become interspersed within the fibrin, and the thrombus tends to propagate in the direction of blood flow. The changes in the vessel wall can be minimal or can include granulocyte infiltration, loss of endothelium and edema.
Where does deep venous thrombosis occur?
DVT occurs in the veins of the calves, popliteal, femoral, and iliac vessels
What are the factors that predispose to venous thrombosis? What are the factor that slows venous flow?
(1) stasis of blood flow (2) hypercoagulability (3) vascular damage. Stasis disrupts laminar flow and brigs platelets into contact with the endothelium. This allows coagulation factors to accumulate and retards the influx of clotting inhibitors. Factors that slow venous flow and induce stasis include immobilization, cardiac failure, and hyperviscosity syndromes
Various clinical disorders cause systemic hypercoagulability, including resistance of coagulation factor V to activated protein C, a prothrombin gene mutation, and inherited deficiencies of antithrombin, protein C, and protein S.
Vascular damage can expose the subendothelial collagen of the endothelium. Exposed collages act as a substrate for the binding of Von Willebrand factor and platelets and initiates the clotting cascade, leading to clot formation.
Less severe damage can cause endothelial dysfunction that contributes to thrombosis by disrupting the production of vasodilating and antiplatelet substance. Atherosclerotic risk factors, such as hyperlipidemia and diabetes are associated with DVT formation.
What is the clinical presentation of deep venous thrombosis?
DVT can be asymptomatic, patient may describe calf or thigh discomfort when standing or walking. The physical signs or proximal DVT include edema of the involved leg and localized warmth and erythema. Calf pain produced by dorsiflexion of the for is a nonspecific and unreliable market of DVT.
How to diagnos a deep venous thrombosis?
Primary laboratory test for the diagnosis of DVT – measurement of the serum D-dimer level and venous compression ultrasonography.
- D-dimer is a byproduct of fibrin degradation that can be measured in a peripheral blood. D-dimer may also be elevated in other conditions (such as cancer, inflammation, infection and necrosis).
- Venous compression duplex ultrasound the criteria used for diagnosis include the inability to compress the vein with direct pressure, direct visualization of the thrombus, and the absence of blood flow within the vessel.
MR venography can be used in the diagnosis of proximal DVT, particularly pelvic vein thrombi, which are difficult to detect by ultrasound.
How to treat a deep venous thrombosis?
Elevation of the affected extremity above the level of the heart helps reduce edema and tenderness, and anticoagulation prevents extension of the thrombus and PE.
- Initial anticoagulation includes low molecular weight heparin (LMWH) and intravenous unfractionated heparin.
- Warfarin, an oral anticoagulant, is then prescribed for long-term management and is continued for several months.
- Catheter-based thrombolysis can be used in patients with iliofemoral deep vein thrombosis.
Treatment against DVT is appropriate in clinical situations in which the risk of developing the condition is high, such as during bed rest following surgery. This include subcutaneous unfractionated heparin, LMWH, low-dose oral warfarin.
what are the risk factors to develop deep venous thrombosis? Which group suffers the most?
The risk of venous thrombosis is high after fractures of the spine, pelvis, and bone of the lower extremities. This is due to the stasis of blood flow, increased coagulability and possibly traumatic endothelial damage.
Women have a higher risk for venous thrombus formation. In the third trimester, the fetus compresses the inferior vena cava and cause stasis of blood flow, and high levels of circulating estrogen may induce a hypercoagulable state. Oral contraceptive (estrogen) product also predispose to thrombus formation.
What is pulmonary embolism epidemiology, etiology and pathophysiology?
PE occurs when a clot dislodges and travels through the inferior vena cava and right heart chamber to the pulmonary vasculature. Gas exchanges is often impaired because of the associated anatomic dead space and ventilation-perfusion mismatch. Pulmonary vascular resistance may rise as a consequence of the mechanical obstruction and because vasoactive and bronchoconstrictive mediators released by platelets within emboli induce constriction of the pulmonary vasculature and bronchospasm. The increased pulmonary vascular resistance may lead to elevation of right ventricular wall stress, dilatation, and contractile failure, compromising cardiac output. Chronic PE can cause remodeling of the pulmonary vasculature with pulmonary hypertension leading to right-sided heart failure.
What is pulmonary embolism clinical presentation?
Dyspnea, pleuritic chest pain, hemoptysis, cough, or fainting (syncope) (due to reduce cardiac output). Signs may include tachypnea, bronchospasm, and evidence of elevated pulmonary artery pressure, including an accentuated pulmonic component of the second heart sound and jugular venous distention.
