Assignment: NURS 6501 Advanced Pathophysiology

Question 1

High-density lipoprotein (HDL) is referred to as good cholesterol. HDL is a cholesterol-rich lipoprotein that transports cholesterol from the body tissues to the liver. HDL exerts an anti-atherogenic effect and reduces cholesterol from the artery walls (Jomard & Osto, 2020). Thus, a low concentration of HDL is associated with atherosclerosis.

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Question 2

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Atherosclerosis is a type of arteriosclerosis that occurs due to plaque formation within the arterial wall. Atherosclerosis occurs from the damage of blood vessels resulting in an inflammatory response. After inflammation of the vessel, a fatty streak surfaces on the inner lining of the artery. Cellular proliferation occurs, resulting in collagen migrating over the fatty streak and forming a fibrous plaque (Asada et al., 2020). The fibrous plaque is usually elevated and protrudes into the vessel lumen, partially or completely hindering blood flow through the artery, which results in atherosclerosis.

Question 3

A pleural friction rub is characterized by an adventitious breath sound heard during chest auscultation as a harsh, grating sound in systole and diastole. The APRN will recognize that SLE caused an inflammation of the pericardium, causing pericarditis. The antigen-antibody complexes formed when the patient was in active lupus-mediated inflammation of the pericardium (Dein et al., 2019). Thus, the APRN should identify that the patient’s clinical features are due to pericarditis, which manifests with fever, tachycardia, dyspnea, and decreased heart sounds. A pericardial rub is a common physical exam finding.

Question 4

DVT is characterized by the presence of a thrombus in a deep venous channel that transports blood to the heart. The patient’s DVT can be attributed to venous stasis, activation of blood coagulation, and damage to the vein. Venous stasis in the patient is likely due to damage to the vein during the hip replacement. Immobility of the left lower extremity could have also caused venous stasis. The venous stasis resulted in an increased viscosity causing the formation of microthrombi, which were not cleared by fluid movement due to high viscosity (Borgel et al., 2019). A blood clot later forms from the microthrombi, blocking blood flow in the vein.

Question 5

Emphysema is characterized by abnormal permanent enlargement of the air spaces adjacent to the terminal bronchioles. It is accompanied by damage to the alveolar walls and increased fibrosis of the alveoli. Emphysema occurs due to impaired gas exchange when the walls of over-distended alveoli are damaged (Rodrigues et al., 2021). As the alveolar walls get damaged, the alveolar surface area in direct contact with the pulmonary capillaries constantly decreases. This results in increased dead space and impaired oxygen diffusion, causing hypoxemia later in the disease. The destruction of lung parenchyma in emphysema is connected to COPD as it causes expiratory airflow limitations (Rodrigues et al., 2021).

References

Asada, Y., Yamashita, A., Sato, Y., & Hatakeyama, K. (2020). Pathophysiology of atherothrombosis: Mechanisms of thrombus formation on disrupted atherosclerotic plaques. Pathology international, 70(6), 309–322. https://doi.org/10.1111/pin.12921

Borgel, D., Bianchini, E., Lasne, D., Pascreau, T., & Saller, F. (2019). Inflammation in deep vein thrombosis: a therapeutic target?. Hematology, 24(1), 742-750. https://doi.org/10.1080/16078454.2019.1687144

Dein, E., Douglas, H., Petri, M., Law, G., & Timlin, H. (2019). Pericarditis in Lupus. Cureus, 11(3), e4166. https://doi.org/10.7759/cureus.4166

Jomard, A., & Osto, E. (2020). High Density Lipoproteins: Metabolism, Function, and Therapeutic Potential. Frontiers in cardiovascular medicine, 7, 39. https://doi.org/10.3389/fcvm.2020.00039

Rodrigues, S. O., Cunha, C., Soares, G., Silva, P. L., Silva, A. R., & Gonçalves-de-Albuquerque, C. F. (2021). Mechanisms, Pathophysiology and Currently Proposed Treatments of Chronic Obstructive Pulmonary Disease. Pharmaceuticals (Basel, Switzerland), 14(10), 979. https://doi.org/10.3390/ph14100979

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Assignment: NURS 6501 Advanced Pathophysiology