Disorders of the Veins and Arteries

Introduction

Advanced practice nurses often encounter patients who present with vein and artery disorders, which could be life threatening. The most common diseases in this context are chronic venous insufficiency (CVI) and deep venous thrombosis (DVT). Due to the difficulties that are associated with the diagnosis of the disorders, it is important for nurses to examine clinical signs of patients thoroughly in order to treat the right condition. This paper aims at achieving three objectives. First, it will compare CVI and DVT as well as contrast venous thrombosis and arterial thrombosis. Second, the essay will discuss age with regard to how it can affect the two disorders and how to diagnose and offer medications on the premises of age. Third, it will construct two mind maps of CVI and DVT on the premises of the pathophysiology, epidemiology, diagnosis and treatment.

Similarities between CVI and DVT

Chronic venous insufficiency (CVI) is a health condition that occurs when blood that has insufficient oxygen goes back to the heart. Thus, it stagnates in the veins and it causes swelling. This blood causes swelling of vena cava and pain. The clots can break away and lodge in the lung, causing a condition known as pulmonary embolism (Huether & McCance, 2012, p. 585). CVI results from improper functioning of vein valves, leading to blood circulation impairment. This occurs mainly due to damaged and blocked valves. Just like CVI, DVT clotting of blood in veins causes the condition. The condition results from lengthy periods of bed confinement (McPhee & Hammer, 2012, p. 197). DVT potentially leads to valve damages and blockages leading to CVI (Huether & McCance, 2012, p. 586). Thus, it is clear that both CVI and DVT affect veins and they result from blockage of the pathways that are essential in the transport of blood.

Contrasts between venous thrombosis and arterial thrombosis

The two disorders of blood vessels differ in multiple ways. Arterial thrombosis results from existing vascular abnormalities/diseases. It affects medium to large sized arteries. Conventionally, it affects femoral, carotid, coronary, cerebral, and renal arteries (Jenkins, Rawley, Smith & O’Donnell, 2012, p. 653). A white clot forms in arterial thrombosis. Scientists argue that arterial thrombosis occurs in response to endothelial cell injuries. Clotting exhibited in arterial thrombosis occurs when injured circulation platelets interact with sub-endothelium/atherosclerotic plaque.

Venous thrombosis records substantial differences in blood clotting pathology compared to arterial thrombosis. Unlike white clots in the case of arterial thrombosis, venous thrombosis clots. Healthcare professionals call these formations red clots. These clots are larger compared to the white clots. They are made of fibrin that is rich in cell elements (Jenkins et al., 2012, p. 655). The clot formation result from stasis and variations in the composition of blood.

The age factor

It is important to note that both disorders have correlations with patient factors. One such factor is age. Multiple researchers argue that the risk of CVT and DVT increases exponentially with age (Jenkins et al., 2012, p. 658). In fact, some researchers have linked life expectancy increase to increased cases of CVT and DVT (Silverthorn, Ober, Garrison, & Silverthorn, 2009, p. 124).

Further, a major protein known as Willebrand factor (vWF) found in the platelet-vessel increases with age. For example, research has shown that fibrinogen’s plasma levels rise from 285 mg/dl in people aged 45-55 years to 310 mg/dl for people aged 66-80 years (Silverthorn et al., 2009, p. 140). This increased level of fibrinogen in plasma is widely believed to have a causative effect in high cardiovascular cases among the elderly. Additionally, coagulation factor VII, rises as age increases (Silverthorn et al., 2009, p. 170). This factor’s role in coagulation is undisputed. Further, rise in platelet reactivity as one grows old is common. The reactivated platelets accelerate generation of thrombin (Sherwood, 2011, p. 103).

Clinical assessment is not sufficient to achieve holistic diagnosis. Leg pain and difficulty in walking are the first signs of these conditions. Ultrasound is a vital tool in diagnosis. The Wells pre-test is an important factor in the diagnosis of the disorder. The test is reportedly superior to clinical analysis. For suspected cases of DVT and CVI, d-dimers are essential features in diagnosis. However, for patients with intermediate to high pre-test probability as well as those who show a positive d-dimer, ultrasound is the best diagnostic test (McPhee & Hammer, 2012, p. 199).

Mind maps

A diagram showing the mind map of CVI. It shows the pathophysiology, epidemiology, diagnosis and treatment of the condition.
Figure 1. A diagram showing the mind map of CVI. It shows the pathophysiology, epidemiology, diagnosis and treatment of the condition.

Mind map of DVT

A diagram showing the mind map of DVT. It shows the pathophysiology, epidemiology, diagnosis and treatment of the condition.
Figure 2. A diagram showing the mind map of DVT. It shows the pathophysiology, epidemiology, diagnosis and treatment of the condition.

Conclusion

Advanced practice nurses are required to understand the various aspects that are critical in comprehending the clinical presentations of CVI and DVT. A thorough understanding of the aspects is also important in adopting the best treatment approaches that could result in improved outcomes. Both disorders involve blockage of blood vessels, but CVI blocks veins close to the skin surface while DVT blocks deep veins. Early diagnosis is an important strategy that helps to prevent the disorders from causing serious effects on patients. At advanced stages, surgery to remove clots could be required.

References

Huether, S. E., & McCcance, K. L. (2012). Understanding pathophysiology (Laureate custom ed.). St. Louis, MO: Mosby. Web.

Jenkins, P. V., Rawley, O., Smith, O. P., & O’Donnell, J. S. (2012). Elevated factor VIII levels and risk of venous thrombosis. British journal of haematology, 157(6), 653- 663. Web.

McPhee, S. J., & Hammer, G. D. (2012). Pathophysiology of disease: An introduction to clinical medicine. New York, NY: McGraw-Hill Medical. Web.

Sherwood, L. (2011). Human physiology: from cells to systems. Boston, MA: Cengage Learning. Web.

Silverthorn, D. U., Ober, W. C., Garrison, C. W., & Silverthorn, A. C. (2009). Human physiology: an integrated approach. Hoboken, NJ: Pearson/Benjamin Cummings. Web.