Hashimoto's Thyroiditis Case Study Essay

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Hashimoto’s thyroiditis Case Study “Pathophysiology refers to the study of abnormalities in physiologic functioning of living beings” (Copstead and Banasik, 2013, p.1). Pathophysiology attempts to discover any responses and reactions of living being’s organs, tissues, cells and body fluids, in response changes experienced in its internal or external environment. Pathophysiology becomes extremely important in the medical setting as it allows us to predict expected outcomes of diseases while giving the medical team a general overview of signs and symptoms, identifying the cause, and being able to implementing a treatment to improve, stabilize, or cure disease. A 51-year-old female was admitted to the medical surgical floor at Whittier …show more content…
The patient presented with difficulty swallowing and talking, and stated that over the past 19 months she has gained 40 kilograms and has noticed her hands, face and neck have become swollen and has felt that she is constantly fatigued and unable to carry out her normal daily activities. Upon admission she was noted to have a blood pressure of 160/90, heart rate 55-60, afebrile with no signs of infection. Abnormal lab work showed T4 2000 IU mL, normal being (8000 IU mL, normal being (<1.0 IU L normal being (1.0-negative). The pathophysiology, etiology, incidence and prevalence, signs and symptoms, treatment and plan of care for Hashimoto’s Thyroiditis will be discussed in the next …show more content…
Hashimoto’s thyroiditis sets in once the initial stage, central stage, and final stages have been achieved. According to Chistiakov (2005), in the initial stage “antigen-presenting cells (APC), mostly dendritic cells and macrophage derived, infiltrate the cell” (p. 4). The infiltration of these cells to the thyroid can be activated by environmental factors such as toxins, drugs, iodine consumption, and virus or bacterial infections, which is known as the initial insult to the thyrocytes that begins the autoimmune cascade leading to destruction of the thyroid gland by releasing thyroid specific proteins. According to Chistakov (2005) these thyroid specific proteins “serve as a source of self-antigenic peptides that are presented on the cell surface of APC after processing, which then travel from the thyroid to the draining lymph node” (p. 4). The central stage is described by the unrestrained creation of self-reactive cells and autoantibodies that occur because of the presence of antigens. Stimulated B-lymphocytes make antithyroglobulin (TGAB) and antithyroid peroxidase (ATPO) antibodies, which are focused, against thyroid cells. Autoreactive T-cells, which are produced in the disease process, infiltrate the thyroid

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