Disorders of the Veins and Arteries
Chronic venous insufficiency and deep venous thrombosis are critical disorders of the arteries and veins. Both diseases have varying pathophysiology and understanding them is vital for the proper management and treatment. This paper aims at discussing chronic venous insufficiency and deep venous thrombosis and coming up with their mind maps.
Pathophysiology of chronic venous insufficiency and deep venous thrombosis
The most common pathway that results to CVI (Chronic Venous Insufficiency) is venous hypertension development. Most commonly, venous hypertension is as a result of venous flow obstruction, venous valves’ dysfunction, and venous pump’s failure. During these cases, there is an abnormal flow to the superficial from the deep system. This leads to the production of inflammation fibrosis in the local tissue as well as occasional ulceration.
There are a number of mechanisms that are associated with the failure of the superficial venous valves. In most cases, vein walls that are congenitally weak dilate in normal pressures and lead to secondary valve failure. Superficial phlebitis and direct injury may lead to primary valve failure. Valves that congenitally abnormal are incompetent at ordinary superficial venous pressure. Normal valves and normal veins may be distensible excessively if influenced by hormones (Eberhardt & Raffetto, 2005).
High venous pressure is accountable for various venous insufficiency syndrome’s aspects. If under normal conditions, there are two principal mechanisms that operate to curb venous hypertension. The veins’ bicuspid valves hinder venous pooling and backflow. Again, in cases of normal ambulation, calf muscles reduce venous pressures. Diseased veins’ venous hypertension causes CVI through a number of events.
Usually, deep venous thrombosis (DVT) begins in the calf veins and, thereby, grows in the venous flow direction and towards the heart. If DVT fails to grow, there can be natural clearance and dissolution in the blood, which is referred to as fibrinolysis. The thigh or calf veins are affected most including iliofemoral, popliteal, and femoral vein. If lower-extremity DVT is extensive, it can reach the inferior vena cava and pelvis’ iliac vein. The beginning of the disease is thought to be tissue factor that results to prothrombin being converted to thrombin. Fibrin deposition follows after this. Fibrin and red blood cells majorly form the venous thrombi. Fibrin attaches to the endothelium, a surface that is meant for preventing clotting. White blood cells and platelets are components as well (López, Kearon & Lee, 2004). Although platelets plays a role in the resolution and formation of venous clots, they are not very prominent.
Normally, DVT starts in veins’ valves. The valves’ blood flow pattern can result to blood’s low oxygen concentrations in a valve sinus. This is referred to as hypoxemia and venous stasis worsens it. It also activates pathways such as early-growth-response protein 1 and hypoxia-inducible factor-1. As a result of hypoxemia, there can be reactive oxygen species’ production that activates these pathways, in addition to the nuclear factor-κB that regulates the hypoxia-inducible factor-1 transcription. Early-growth-response protein 1 and hypoxia-inducible factor-1 lead to the association of monocyte with endothelial proteins including P-selectin, which prompts monocytes to produce tissue factor-filled microvesicles. These start clotting following binding in the endothelial surface (López, Kearon & Lee, 2004).
How venous thrombosis is different from arterial thrombosis
Arterial thrombosis is when blood stops to flow from the heart to other body parts. As a result, a person suffers from tissue death. When the arteries carrying blood to the heart die, there is heart attack while gangrene occurs when the arteries in the legs die. On the other hand, venous thrombosis occurs within the veins that return blood to a person’s heart. If this happens in the deep veins, it is acknowledged as a grave matter that necessitates anticoagulation. When on the superficial veins, they appear red and painful.
Diagnosis and treatment
Pregnancy is a patient factor that is present in both DVT and CVI. In DVT, pregnancy escalates the pressure of the legs and pelvis veins. Women suffering from inherited clotting disorder are particularly at risk. The blood clots during pregnancy are a risk that can progress up to six weeks following childbirth (López, Kearon & Lee, 2004).
As far as CVI is concerned, puerperium and pregnancy are significant venous system’s periods in the lower limbs. During pregnancy, there is increased venous pressure as a result of increased blood volume (Eberhardt & Raffetto, 2005). The iliac veins’ compression during the later stages of pregnancy is considered a vital factor. Presently, it is believed that CVI develops or aggravates during pregnancy due to hormonal influence as estrogens reduce the venous wall’s smooth muscle tone.
During pregnancy, DVT is diagnosed though completing a physical examination and medical history. Other diagnostic procedures include duplex ultrasound and venogram. Duplex ultrasound assesses the structure and blood flow in the leg veins. B-mode and Doppler are the two ultrasound modes that are used (López, Kearon & Lee, 2004). Venogram uses intravenous contrast dye and x-rays in visualizing veins. The treatment of DVT during pregnancy encompasses the use of thrombolytic therapy, anticoagulation therapy, and inferior vena cava filter insertion.
CVI can be treated through a number of strategies including limb elevation, surgical litigation, heparin therapy, wearing compression stockings, and stripping and conservative vein resection. The disease is effectively treatable during the initial stages. A combination of treatments is usually recommended. The diagnosis involves a physical exam and medical history analysis. A duplex or vascular ultrasound examines blood circulation in the legs (Eberhardt & Raffetto, 2005).
From the foregoing discussion, it is evident that chronic venous insufficiency and deep venous thrombosis are critical diseases of the arteries and veins and they can be managed through a number of ways. There are a number of patient factors and a healthy lifestyle that encompasses of physical exercise and proper diets is vital for preventing these diseases.
Eberhardt, R. T., & Raffetto, J. D. (2005). Chronic venous insufficiency. Circulation, 111(18), 2398-2409.
López, J. A., Kearon, C., & Lee, A. Y. (2004). Deep venous thrombosis. ASH Education Program Book, 2004(1), 439-456.