Chronic venous insufficiency and deep venous thrombosis pathophysiology

Disorders of the Veins and Arteries

Chronic venous insufficiency and the deep venous thrombosis fall within the most common medical issues that the adult population is vulnerable to. These disorders have very common symptoms but mostly those symptoms are mistakenly diagnosed for a different medical problem. Earlier these disorders were thought to be of a simple nature but recent researches have shown that the cellular and molecular aspects of these disorders show 'complex multifactorial processes are reflecting both systemic abnormalities of connective tissue synthesis and cellular inflammatory reaction.' (Chieh-Min Fan, 2005).

Pathaphysiology of CVI and DVT

It is believed that the chronic venous insufficiency (CVI) in the veins occurs primarily because of the weakness of the vein walls. A regular normal vein includes compliance providing elastic fibers, strength providing collagen matrix, and three layers of smooth muscle that aid in controlling the tone of the vein. In most cases it is understood that the muscle layers' distortion and disruption leads to the proliferation of the collagen matrix. The more the infected area, the more are the disrupted muscle layers, leaving the collagen matrix and the elastic layers vulnerable. As a result of this alteration, the veins lose contractility and result in vessel dilation whilst responding to the hypertension in the veins.

Deep vein thrombosis (DVT) is the clotting of blood in the veins. The parts mostly affected are the thigh and the calf veins in the popliteal vein, iliofemoral vein, and the femoral vein. However, DVT can also occur in arms. The occurrence of DVT in the veins is primarily due to a tissue factor. This factor resultantly converts prothrombin into thrombin, which consequently is followed by the deposition of fibrin. The fibrin and the red blood cells combined, deposit themselves on the endothelium, a wall lining of the blood vessels whose purpose itself is to stop blood clotting (Lopez JA, 2009). This deposition mostly initiates in the valves of the vein. The blood pattern flow in the veins cause the oxygen concentration levels in the blood to fall. Thus, the blood clot begins to grow inside the veins, causing DVT.

Impact of patient age on the path physiology of CVI and DVT

The age factor is critical towards understanding how a disease might impact the sick person and how the person's body would respond to the various treatments applied on it. As mentioned earlier, these disorders are more common in the adult population. In the case of CVI, the vein walls weaken as the age of the person increases. This is due to the reason that the internal system of the person has become old, weak and slow. Consequently, the muscle layers in the veins of an infected area easily breakdown and the growth of CVI is quicker as compared to in a person of young age. Similarly, the DVT is also dependent upon the age of the patient.

Treatment of CVI and DVT based on the age factor

The standard treatment prescribed for DVT is the use of medical drugs such anti-coalgulants that prevents the further clotting of blood, but however doesn't act on the existing clots. However, in elderly patients, the low weight molecular herparin prescribed so that they can endure its effects. Further development of the disease is the best cure at any age. This can be achieved by regularly exercising the calf muscles, and walking few hours a day. This can lead to improved functioning of the calf. Other factors to monitor would be controlling and maintaining as close to normal blood pressure as possible. Patient diagnosed with CVI are recommended to elevate their feet above their thighs when they are in a sitting position and above their heart, when they are lying down. This exercise should be performed three or four times a day in order to reduce/control the swelling in the calf.