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
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The thyroid gland is a butterfly shaped organ that is located in the lower part of the neck. The main function of the thyroid is to secrete hormones mainly thyroxin other wise known as T4 and triodothyronine or T3, that regulate the body’s metabolism, growth and development, and regulate body temperature. Hashimoto’s thyroiditis also known as lymphocytic thyroiditis is the most predominant autoimmune thyroid disorder. According to Zaletel and Gaberscek (2011) “lymphocytic infiltration of the thyroid gland is often followed by a gradual destruction and fibrous replacement of the thyroid parenchymal tissue” (p. 576). As large numbers of white blood cells called lymphocytes aggregate in the thyroid and produce antibodies a chain reaction occurs initiating the autoimmune response. This destruction inhibits the production and release of the hormones T4 and T3. Three main causes have been attributed to the development of Hashimoto’s thyroiditis, including environmental, genetic and endogenous factors. The environmental factors attributed to Hashimoto’s thyroiditis include, low iodine intake, drugs, chemicals, and infections. While the genetic factors include Human leukocyte antigen (HLA) gene, cytotoxic T lymphocyte antigen 4 (CTLA4) gene, protein tyrosine phosphatase nonreceptor-type 22 (PTPN22) gene, vitamin D receptor gene, and cytokine genes. Lastly, …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
The thyroid gland is a butterfly shaped organ that is located in the lower part of the neck. The main function of the thyroid is to secrete hormones mainly thyroxin other wise known as T4 and triodothyronine or T3, that regulate the body’s metabolism, growth and development, and regulate body temperature. Hashimoto’s thyroiditis also known as lymphocytic thyroiditis is the most predominant autoimmune thyroid disorder. According to Zaletel and Gaberscek (2011) “lymphocytic infiltration of the thyroid gland is often followed by a gradual destruction and fibrous replacement of the thyroid parenchymal tissue” (p. 576). As large numbers of white blood cells called lymphocytes aggregate in the thyroid and produce antibodies a chain reaction occurs initiating the autoimmune response. This destruction inhibits the production and release of the hormones T4 and T3. Three main causes have been attributed to the development of Hashimoto’s thyroiditis, including environmental, genetic and endogenous factors. The environmental factors attributed to Hashimoto’s thyroiditis include, low iodine intake, drugs, chemicals, and infections. While the genetic factors include Human leukocyte antigen (HLA) gene, cytotoxic T lymphocyte antigen 4 (CTLA4) gene, protein tyrosine phosphatase nonreceptor-type 22 (PTPN22) gene, vitamin D receptor gene, and cytokine genes. Lastly, …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