The disorders of the arteries and veins are collectively referred to as vascular diseases, which are conditions that affect the named blood vessels. The illnesses are best described as a pathological state that affects both medium and large arteries and veins triggered by the dysfunction of the endothelial cells. The activity of the named group of cells is triggered by factors including pathogens and inflammatory stimuli, resulting in the thickening of blood vessel walls. Hence, plaque is formed, which restricts blood flow and the amount of oxygen and nutrients that reach specific body organs, whereas in certain instances plaque may rupture and result in the formation of clots (Vanhoutte et al., 2017). Thus, this paper will focus on comparing the pathophysiology of two vascular diseases including chronic venous insufficiency (CVI) and deep venous thrombosis (DVT) as well as the assessment of the impact of genetics on their pathophysiology, diagnosis, and treatment.
The pathophysiology of CVI is divided into two categories, reflux, and obstruction. Reflux is characterized by the incompetence of the venous valves and venous hypertension as well as inflammation of vessel walls and hemodynamic factors. The alteration of the stress levels on the vessel walls causes the release of pro-inflammatory messengers in higher quantities. Additionally, in cases that the affected patient is immobile or has stiff joints, the mechanisms named above can be aggravated further by dysfunctional vascular and muscle pumping. Furthermore, obstruction occurs because of thrombosis affecting the deep leg or pelvic veins, which may, in turn, be associated with post-thrombotic syndrome. The combination of obstruction and reflux results in venous ulcers (Santler & Goerge, 2017). Hence, CVI impairs the functioning of perforating vein valves in preventing blood reflux from deep to superficial veins.
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The pathophysiology of DVT is characterized by the manifestation of three factors, including venous stasis, vein damage, and activation of blood coagulation. Venous stasis is triggered by the obstruction of venous blood flow resulting in the formation of microthrombi and increased viscosity, which if not corrected results in the growth and propagation of the thrombus. Moreover, endothelial damage in the blood vessel may result from internal or external trauma, causing a hypercoagulable state seeded by the imbalance of biochemical factors (Patel, Chun & Brenner, 2019). Therefore, a comparison of the pathophysiology of CVI and DVT evidences that while CVI impairs valve functions, which in turn affect venous activities, DVT directly impacts the operations of the vein.
An assessment of arterial and venous thrombosis establishes that the former results from blood clots that block arteries from carrying oxygenated blood from the heart to other body parts, whereas the latter is caused by coagulate that mitigates the transportation of de-oxygenated blood from the body to the heart. Moreover, arterial thrombosis occurs when blood has a high flow rate causing thrombi that are rich in platelets to form around damaged endothelium and atherosclerotic plaques. In turn, venous thrombi form under low blood pressure and are characterized by the encapsulation of red blood cells and activated platelets in fibrin (Chan, Eikelboom & Weitz, 2016). Hence, the type of blood flow in the arteries and veins determines the nature of the thrombi formed.
Genetics may affect the pathophysiology of CVI in a case that the affected patient has mutated FOXC2 genes. The named hereditary units are vital to the development of venous valves, and their mutation can result in the malfunction of vein valves (Boisseau, 2014). The diagnosis of CVI in a patient with the stated genetic variation would be based on the determination of the disease’s phenotype including components such as its severity, anatomy, and varicosity (Krysa, Jones & Van, 2012). The best treatment option for FOXC2-based CVI would be Radiofrequency (RF) Vein Ablation, which is a minimally invasive operative procedure that allows doctors to eliminate venous reflux by heating up and damaging the wall inside the affected vein using radiofrequency energy. Following the stated treatment, the patient may require to wear compression stockings to facilitate the recovery process (Kayssi et al., 2015). In the case of CVT, the FV Leiden genetic mutation may affect the pathophysiology of the disease. FV Leiden increases the predisposition to DVT because of the abnormal effect it has on blood clotting resulting in thrombophilia. The diagnosis of the gene-based variant of DVT would be based on the patient’s medical history, a D-dimer test, clinical findings, assessment for gene mutations and a Doppler ultrasonography to confirm the results ( Hosseini et al., 2016) . The most efficient form of treatment for a patient with DVT caused by the presence of FV Leiden would be consistent anticoagulant treatment to reduce the risk of venous blood clotting ( Bezgin et al., 2018) . Thus, effective treatment of vascular diseases such as CVI and DVT requires the assessment of its properties, including the causative factor associated with heredity.
References
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