Understanding the clinical manifestation of imbalance in human anatomy and how to differentiate groups of symptoms into disease processes is essential for an advanced practice nurse in making an accurate decision for diagnosis and treatment therapies. One of the aspects that nurses should understand is the bodies’ circulatory system, particularly the venous system. This paper covers the pathophysiology and genetic influences of chronic venous insufficiency (CVI) and deep vein thrombosis (DVT). The paper also identifies key distinctions between DVT and arterial thrombosis and provides a mind map for two venous disorders.
Pathophysiology of CVI and DVT Comparison
CVI pathogenesis is connected to venous reflux and obstruction or in some cases a combination of both. Venous has several mechanisms that are based on key elements, including venous vale ineffectiveness, hemodynamic elements, vessel wall swelling, and venous hypertension. Blood reflux from deep veins is prevented by perforating veins valve from flowing into superficial veins (McPhee, & Hammer, 2019). The obstruction causes venous blood to reflux backward into already congested veins legs. Congestion of blood results to high hydrostatic venous pressure causing CVI.
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Similarly, DVT also is a result of clotting of blood within a deep vein of a limb, which mostly occurs in the pelvis, a thigh or calf. The clotting of blood causes inflammation of the veins walls, leading to the formation of thrombus. The inflammation eventually venous thrombi that are attached to the vein wall to grow tails and spread them towards the direction of flow to avoid layers of a blood clot formed (Huether, & McCance, 2017). Venous thrombi tails like attachment are made up of red and white blood cells, fibrin, and platelets. The aggregation of tails is critical since it might cause breaking off blood clots, which if travel in the bloodstream might end up blocking other veins. Lower-level extremity DVT in most cases is as a result of damaged venous return, dysfunction due to post-fracture of leg, hypercoagulability, or endothelial injury. However, in concurrent, the upper-level extremity DVT usually is as results of endothelial injury due to pacemakers, injections drug usage, or central venous catheters.
Venous and Arterial Thrombosis Differences
Venous thrombosis involves the clotting of blood a vein while arterial thrombosis is as a result of blood clots developing within an artery. Venous thrombi primarily consist of fibrin and trapped erythrocytes such as platelets and are formed in the areas experiencing stasis due to the initiation of the blood coagulation mechanism. The Arterial thrombi are platelets and are formed at sites of vessel-wall injuries that arise when blood flows at high-velocity. The causes of venous thrombosis may include diseases or leg veins injury, immobility, a fracture on the bone, obesity, and use of certain medicines. Venous thrombosis is also as a result of inherited disorders, autoimmune disorders that make it more likely that one’s blood will clot, and medicine that can increase risk of clotting, for instance, certain birth control medicines (Johns Hopkins Medicine, 2019). Arterial thrombosis is caused by arteries hardening a condition known as arteriosclerosis. Arteriosclerosis occurs when artery walls thicken due to fatty or calcium deposits, causing the buildup of fatty material on artery walls that can rupture, resulting in a blood clot. Risk factors for venous thrombosis include a history of DVT, pregnancy, vein injury, blood clotting inherited disorders, older age, smoking, and obesity. The risk factors for arterial thrombosis include diabetes, history of arterial thrombosis, high cholesterol, high blood pressure, poor diet, obesity, and older age.
Genetic Impact on the Pathophysiology of CVI and DVT
Inherited thrombophilia gene mutations play a causative role in venous thromboembolism (VTE) manifestation, which is scientifically proven by DVT. However, several kinds of research have established the difference in the occurrence of VTE based on races. Studies indicate that a high frequency of 4G allele is common in patients who experience DVT. For instance, a Chinese study analyzing hereditary nature of varicose veins established that nuclear families compatible with autosomal dominant inheritance had 70% t0 90% penetrance, and 37% sporadic cases were consistent with autosomal receive inheritance (Boisseau, 2017). Varicose vein diseases were connected to the candidate marker D16S520 on chromosome 16q24, indicating linkage to fox headbox protein C2 (FOXC2) transcription factor. FOXC2 gene mutations are connected with the lymphedema- distichiasis syndrome, which is commonly observed as varicose veins phenotypic irregularities at a young age. Therefore, there is a possibility of FOXC2 gene role in the development of varicose vein and failure of the lymphatic system.
Diagnosis and Treatment of CVI and DVT
The diagnosis of Chronic Venous Insufficiency (CVI) relies on history, clinical presentation, and diagnostic procedures. Diagnostic procedures that can be employed include continuous-wave Doppler ultrasound with the use of a pencil probe that allows exploratory and inexpensive leg veins examination (Santler & Goerge, 2017). Color-flow duplex ultrasound can also be used to provide for morphological and functional assessment of the venous system. Diagnostic procedures can also be conducted using phlebography X-ray technique. Treatment of CVI involves several options including the use of conservative treatment which consists of compression therapy and supportive measures like manual lymphatic drainage, physical therapy, and phlebotonics. Other treatment options are sclerotherapy, surgical procedures, endovenous thermal and chemical procedures, and novel procedures.
Diagnosis of DVT is conducted through ultrasonography, which recognizes thrombi by unswervingly visualizing the venous lining and indicating impaired or abnormal venous flow. Another diagnostic method used is D-Dimer testing. Negative D-Dimer level is used to identify patients with low DVT probability while the positive level is used to confirm the diagnosis (Douketis, 2019). The treatment of lower and upper extremity DTV aims at Pulmonary Embolism (PE) prevention and prevention of the occurrence of DTV, CVI, and postphlebitic syndrome. The treatment options comprise the use of anticoagulation therapy, thrombolytic therapy, and surgery.
References
Boisseau, M. (2017). Chronic venous disease and the genetic influence. Phlebolymphology.org . Retrieved from https://www.phlebolymphology.org/chronic-venous-disease-and-the-genetic-influence/
Douketis, J. (2019). Deep Venous Thrombosis (DVT). Merck Sharp & Dohme Corp . Retrieved from https://www.msdmanuals.com/professional/cardiovascular-disorders/peripheral-venous-disorders/deep-venous-thrombosis-dvt#v37965446
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Johns Hopkins Medicine. (2019). Thrombosis . Retrieved from https://www.hopkinsmedicine.org/health/conditions-and-diseases/thrombosis
Hammer, G. D., & McPhee, S. J. (2019). Pathophysiology of disease: An introduction to clinical medicine (8th ed.). New York, NY: McGraw-Hill Education.
Santler, S., & Goerge, T. (2017, May 09). Chronic venous insufficiency – a review of pathophysiology, diagnosis, and treatment. Journal of German society of Dermatology . https://doi.org/10.1111/ddg.13242
