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don't have time dadsfav96please paraphrase this assignment with no AI use roduction Pulmonary embolism (PE) is a potentially life-threatening condition resulting from obstruction of the pulmonary arterial system, most commonly due to embolization of a thrombus from the deep veins of the lower extremities. Prompt recognition of PE relies on understanding the underlying pathophysiology, associated genetic and acquired risk factors, and patient-specific variables that contribute to disease development. This case study analyzes a 48-year-old female presenting with acute respiratory and cardiovascular symptoms consistent with pulmonary embolism, with emphasis on pathophysiological mechanisms, genetic predisposition, and lifestyle and demographic contributors. Pathophysiological Processes and Diagnostic Significance The patient’s clinical presentation is most consistent with an acute pulmonary embolism secondary to venous thromboembolism (VTE). Pulmonary embolism occurs when a thrombus, typically originating in the deep veins of the lower extremities, dislodges and travels to the pulmonary circulation. In this case, the patient’s unilateral right calf swelling for several days suggests deep vein thrombosis as the embolic source. Obstruction of pulmonary arteries leads to ventilation–perfusion mismatch, resulting in impaired oxygen exchange and hypoxemia, as evidenced by the patient’s oxygen saturation of 88% on room air. Increased pulmonary vascular resistance causes right ventricular strain and sympathetic activation, explaining the tachycardia, tachypnea, hypotension, and anxiety. The sharp, pleuritic chest pain that worsens with inspiration reflects pleural irritation or pulmonary infarction. The sudden onset of symptoms in the absence of infection strongly supports pulmonary embolism as the primary diagnosis. Genetic Mutations and Risk Factors Inherited thrombophilias increase the risk of venous thromboembolism by promoting a hypercoagulable state. Common genetic mutations include Factor V Leiden, prothrombin gene mutation (G20210A), and deficiencies of protein C, protein S, or antithrombin. These abnormalities impair natural anticoagulant pathways, increasing the likelihood of thrombus formation. Although this patient has no documented genetic history, the development of VTE at a relatively young age may warrant further evaluation. The patient also possesses multiple acquired risk factors, including obesity, hypertension, and the use of combined estrogen–progestin oral contraceptives. Estrogen increases clotting factor production while reducing anticoagulant proteins. Prolonged immobility during an eight-hour flight further promoted venous stasis. These factors collectively increased the patient’s susceptibility to pulmonary embolism. Racial/Ethnic Variables and Lifestyle Factors Racial and ethnic variables may influence the incidence and outcomes of venous thromboembolism due to genetic differences and social determinants of health. Individuals of African ancestry experience higher VTE rates and worse outcomes, while inherited thrombophilias such as Factor V Leiden are more prevalent among individuals of European descent. Although the patient’s race is unspecified, awareness of these differences is important in clinical evaluation. Several lifestyle factors contributed to disease development. A sedentary occupation, prolonged air travel, obesity, varicose veins, and oral contraceptive use collectively created an environment of venous stasis and hypercoagulability, leading to thrombus formation and pulmonary embolism. Summary This case demonstrates a classic presentation of acute pulmonary embolism driven by venous stasis, hypercoagulability, and endothelial dysfunction. The patient’s symptoms are directly explained by the underlying pathophysiology of pulmonary arterial obstruction and impaired gas exchange. Recognition of genetic and acquired risk factors is essential for accurate diagnosis, timely intervention, and prevention of recurrent events.

References

Konstantinides, S. V., et al. (2020). 2019 ESC guidelines for the diagnosis and management of acute pulmonary embolism. European Heart Journal, 41(4), 543–603. https://doi.org/10.1093/eurheartj/ehz405 Kearon, C., et al. (2021). Antithrombotic therapy for VTE disease: Updated guidelines. Chest, 160(6), e545–e608. https://doi.org/10.1016/j.chest.2021.07.055 Stone, J., et al. (2020). Deep vein thrombosis: Pathogenesis, diagnosis, and medical management. Cardiovascular Diagnosis and Therapy, 10(3), 821–836. https://doi.org/10.21037/cdt.2020.03.01

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