Application: Disorders of the Veins and Arteries

Answer

Comparison between the Pathophysiology of Chronic Venous Insufficiency and deep Venous Thrombosis

            In chronic venous insufficiency pathophysiology, there is increased venous pressure, which is by far largely responsible for various aspects associated with venous insufficiency disorder. When the body is functioning normally as expected, two mechanisms are known to act as safeguards against venous hypertension including vein’s bicuspid valves, which prevent venous pooling as well as backflow. In addition, when normal ambulation is happening calf muscles are known to decrease pressures by an approximated 70 percent. In affected veins, however, ambulation lowers venous pressures by just 20 percent. This has been viewed to likely lead to venous hypertension and in diseased veins, it is viewed to lead to Chronic venous insufficiency. Some of the major events involved include raised venous pressure transcending the venules to bodily capillaries and thus curbing flow, in turn, low flow states lead to leukocyte trapping and further leading to release of harmful oxygen free radicals as well as proteolytic enzymes, fibrin cuff formation, and inflammation as well as tissue loss emerge (Huether and McCance, 2013). It must be noted that in most cases the failure of vein valve take place following primary points of increased pressure leakage emerge between the superficial and the deep system. This increased pressure brings about failure of secondary valve when otherwise normal functionality would see veins become widely dilated to ensure that the thin flaps cannot make contact touch vessel’s lumen. Increased pressure leakage out of the deep veins to the deep and the superficial system can result from perforator as well as functional valve failure. In addition, poor clearance of carbon dioxide, lactate, and other cellular respiration products may contribute to the emergence of this syndrome.

In comparison, deep venous thrombosis has venous stasis, blood coagulation activation, as well as vein damage as the three leading factors. The physiological transformations can emerge due to therapies, treatments, as well as pathology. It can be said that similar to chronic venous insufficiency, deep venous thrombosis by far and large results out of impaired venous return as well as endothelial dysfunction. Indeed, thrombosis relates to the homeostatic mechanism in which blood clots, which is crucial to the development of homeostasis following a wound. Though this process may be initiated through various pathways, the mechanisms often comprise of cascading enzyme activation, which magnify the impact of the first trigger event. Similarly, complex events lead to fibrinolysis and the formation of microscopic thrombus is a continous event (Huether and McCance, 2013). By far and large, the clot mechanism comprises of a sequence of self-regulating procedures that lead to the creation of a fibrin coagulate. Generally, the start of the coagulation process can be divided into two parts including intrinsic as well as extrinsic system. The latter functions due to activation through tissue lipoprotein, which is often released due to mechanical injury. On the other hand, the intrinsic system often is about circulating plasma factors. Nevertheless, once a fibrin coagulate is developed and it has undertaken its homestasis function, there are bodily mechanisms meant to restore normal flow. In fact, a physiologic balance between factors promoting and those that retard coagulation normally exists. Yet, a disturbance in the balance may lead to the clotting process taking place in an excessive manner. Often, deep venous thrombosis happens behind valve cusps and venodilation may upset the endothelial cell barrier as well as expose the subendothelium. Neutrophils as well as platelets are activated to release inflammatory mediators. Altogether, thrombus organization kicks off with inflammatory cells being infiltrated into the coagulate leading to a fibroelastic intimal coagulating at the place of thrombus attachment. In patients, the interaction between thrombus and vessel wall causes valvular dysfunction as well as general wall fibrosis in veins. Over months, most acute deep venous thrombosis evolves to total or partial recanalization.

How Venous Thrombosis is different from Arterial Thrombosis

            Venous thrombosis differs from arterial one in that venous thrombosis is by far and large a matter of clotting system activation whereas arterial thrombosis largely is a phenomenon relating to platelet activation (Lijfering et al, n.d). In fact, arterial thrombi is known to take place at areas in which plaques are created as well as places in which sheer stress is high leading to platelet rich white thrombi. Venous thrombi, on the other hand, tend to take place at areas in which the vein wall in intact and in which blood flow as well as sheer stress is low leading to red cell rich named red thrombi.

How the patient factor might impact the pathophysiology of CVI and DVT

            The selected patient factor is age. This factor impacts the pathophysiology of DVT because being in excess of 60 years increases the risk of DVT (Davies and Lumsden, 2011). In fact, persons exceeding this age limit often suffer from immobilization and lower extremity DVT is known often to result out of impaired venous return including in immobilized persons or patients. In addition, older persons often suffer from several conditions such as hypertension. In fact, hypertension is increasingly linked to increasing age, which is similar to the occurrence of venous thrombosis. On the other hand, age impacts the pathophysiology of age impact the pathophysiology of CVI through increased likelihood of age impact the pathophysiology of CVI with increased age. In fact, age is among the known risk factors of CVI due to increased probability of decreased bodily function as age increases.

I would diagnose as well as prescribe treatment of the disorders for a patient based on age keeping in mind that older persons tend to suffer from other disorders that may accelerate or even make diagnosis more complex. For instance, it is crucial to follow the history of older patients regarding hypertension as this may make treatment even more complex.