The Causes and Effects of Hyperthyroidism - Case Study Example

The Causes and Effects of Hyperthyroidism Name Course Institution Date Abstract The purpose of this paper is to discuss the causes and effects of hyperthyroidism. The content of the paper is researched from credible peer reviewed journal articles. The thyroid gland is responsible for the production of thyroid hormones thyroxine (T4) and triiodotyrosine (T3). These hormones play a great role in metabolism and cell growth and differentiation. The thyroid gland is regulated by the thyroid stimulating hormone (TSH) in the production of these hormones. The TSH is in turn regulated by the hypothalamus produced by the pituitary gland in the brain. Any impairment in the thyroid gland or the thyroid-pituitary feedback mechanism can cause abnormal thyroid function. Abnormal production of thyroid hormones can result to various thyroid conditions including hyperthyroidism. Hyperthyroidism occurs when the thyroid hormones thyroxine and triiodotyrosine are produced in excess. Common causes include Graves’ diseases, toxic adenoma, toxic multinodular goitre, thyroidititis, pituitary tumors, and excess ingestion of iodine. Symptoms include palpitations, tremors, visual problems, weight loss, sweating, increased bowel movement, muscle weakness and fatigue. Diagnosis is achieved through physical observation of symptoms and family history, testing the blood for elevated T4 and T3 and low TSH, and imaging technologies. Treatment is by antithyroid medication, surgery and radioactive iodine. Introduction Hyperthyroidism is a condition that is caused by excessive production of thyroid hormones. To understand the causes and effects of hyperthyroidism, this paper begins by discussing the physiology and function of the thyroid gland. This is followed by the discussion of the pathophysiology of hyperthyroidism in terms of how it manifests and its causes. Symptoms of hyperthyroidism are discussed followed by a discussion of how hyperthyroidism is diagnosed. Lastly, the paper describes the treatment options available in the management of hyperthyroidism these being medication, radiation and surgery. a) Physiology and function of the thyroid gland The thyroid gland wraps around the anterior and lateral surfaces of the pharynx, larynx, esophagus and trachea and forms lobes attached by the isthmus in the front part of the neck (Adelchi et al. 2014). The thyroid gland produces and releases hormones that control metabolism (Maia et al., 2011). These are thyroxine (T4) and triiodotyrosine (T3). T4 and T3 are required for cell homeostasis (Maia et al., 2011). They direct cell differentiation growth and metabolism and are considered the major metabolic hormones as they target nearly every tissue in the body (Maia et al., 2011). The thyroid gland itself is regulated by the pituitary gland located in the brain while the pituitary is controlled also by the thyroid through a negative feedback mechanism, and the hypothalamus in the brain (Hoermann et al. 2013). The hypothalamus releases the thyrotropin releasing hormone (TRH) which signals the pituitary to release the thyroid stimulating hormone (TSH) (Hoermann et al. 2013). The TSH signals the thyroid to release the thyroid hormones T4 and T3 (Khan, 2012). TRH travels through the portal venous system to the adenohypophysis and TSH is produced in the adenohypophysis thyrotrophs (Sirakov & Plateroti 2011). TSH triggers several processes including iodine uptake, colloid endocytosis and growth of the thyroid gland (Sirakov & Plateroti 2011). The biosynthesis of T4 and T3 includes the processes of dietary iodine ingestion, active transport and uptake of iodide by the thyroid gland, and oxidation of iodide and iodination of thyroglobulin tyrosine residues (Pesce & Kopp 2014). The iodotyrosine residues couple to form T4 and T3 and the proteolysis of thyroglobulin releases T4 and T3 into the circulation (Miot et al. 2014). b) Pathophysiology of hyperthyroidism Hyperthyroidism is a condition resulting from abnormal thyroid function. It refers to the synthesis and secretion of excess thyroid hormones T4 and T3 (Dietrich, Landgrafe & Fotiadou 2012). Consequently, metabolism is accelerated. Various conditions cause hyperthyroidism. Major causes of hyperthyroidism include Graves’ disease, hyperfunctioning thyroid nodules, thyroiditis and excess iodine intake (Adelchi et al. 2014). Graves’ disease is an autoimmune disease that tends to be hereditary and occurs mostly in women (Dietrich, Landgrafe & Fotiadou 2012). The antibody thyroid stimulating immunoglobin (TSI) is produced and directed against the TSH receptor (Laurberg 2014). The thyroid gland becomes over stimulated and loses the negative feedback to T4 and T3 leading to their excess secretion. Hyperfunctioning thyroid nodules are characterized by the conditions toxic/functioning adenoma, and toxic multinodular goiter (Miot et al. 2014). This causes hyperthyroidism when single or multiple adenomas in the thyroid produce excess T4 and T3 (Miot et al. 2014). An adenoma is a part of the thyroid gland that has separated itself from the rest of the gland, resulting in benign lumps that may cause an enlargement of thyroid (Lim et al. 2015). Some adenomas do not secret hormones and cannot cause hyperthyroidism. Others become autonomous and produce the thyroid hormones independently while failing to respond to the pituitary regulation via the TSH (Lim et al. 2015). Thyroiditis, an inflammation of the thyroid gland also causes hyperthyroidism by the leaking of T4 and T3 to leak out of the gland in excess (Dietrich, Landgrafe & Fotiadou 2012). The thyroid gland can become inflamed for unknown reasons and this inflammation causes the leak of the hormones. Excess iodine also causes hyperthyroidism (Dietrich, Landgrafe & Fotiadou 2012). Iodine is used in the biosynthesis of T4 and T3 hence its excess availability leads to excess production of T4 and T3 which cause hyperthyroidism. Ingestion of large amounts of tetraiodothyronine either through dietary supplements or medication also causes hyperthyroidism (Dietrich, Landgrafe & Fotiadou 2012). Some tumors are also responsible for hyperthyroidism. Benign tumors in the thyroid or pituitary gland may cause hyperthyroidism by interfering with the production of thyroid hormones (Lim et al. 2015). They stimulate the abnormal excessive production of TSH signaling the thyroid to produce excess T4 and T3 (Miot et al. 2014). Tumors of the reproductive organs - ovaries and testes- may also cause hyperthyroidism. c) Symptoms of hyperthyroidism Symptoms of hyperthyroidism usually relate to increased metabolic rate in the body. The symptoms include changes in neuropsychiatric manifestations including nervousness, agitation, irritability, and mood instability (Hage & Azar 2012). Tremors usually trembling of hand and fingers and decreased concentration are present (Lim et al. 2015). The patient may experience increased appetite but also has sudden weight loss regardless of the amount of food taken (Khan 2012). Other symptoms include increased bowel movements, intolerance to heat, and excessive sweating (Hage & Azar 2012). Tachycardia or rapid heart rates of at least 100 beats per minute and arrhythmia/palpitations are also common hyperthyroidism symptoms (Bielecka-Dabrowa et al. 2009). Fatigue and muscle weakness, especially in thighs and upper arms are also common hyperthyroidism symptoms (Hage & Azar 2012). Other symptoms include changed sleep patterns including insomnia. The skin can become moist and thin (Lim et al. 2015). The hair becomes fine and brittle and hair loss is inevitable (Lim et al. 2015). If Graves’s disease is the primary cause the patient may present with exophthalmos including bulging eyes or unblinking stare (Laurberg et al. 2014). In goiter, the thyroid is visibly enlarged and appears as a swelling at the base of the neck (Laurberg et al. 2014) Women may have irregular periods, usually missed or scant/light periods (Bartalena et al. 2015). Breast enlargement may occur in men with hyperthyroidism (Maia, et al. 2011). Nausea and vomiting are also common symptoms (Sirakov & Plateroti 2011). The symptoms are less noticeable in people with mild hyperthyroidism (Palacios, Pascual-Corrales & Galofre 2011). Patients older than 70 years may also not show the typical hyperthyroidism symptoms (Palacios, Pascual-Corrales & Galofre 2011). Therefore, untreated hyperthyroidism in the old age group may result in a thyroid storm characterized by arrhythmia, high blood pressure, fever and congestive heart failure (Bielecka-Dabrowa et al. 2009). The symptoms also include mental conditions including delirium and confusion (Bielecka-Dabrowa et al. 2009). d) Diagnostic and investigative tests including reference ranges The first step to diagnosing hyperthyroidism is taking the patient’s complete history and physical examination (Palacios, Pascual-Corrales & Galofre 2011). These reveal the common symptoms including weight loss, arrhythmia, elevated blood pressure, protruding eyes and enlarged thyroid gland among others (Palacios, Pascual-Corrales & Galofre 2011). Knowing if there are members of the patient’s family with conditions such as Graves’ disease can contribute to the diagnosis of hyperthyroidism. The most widely used diagnostic test for hyperthyroidism is the thyroid function tests (Hoermann et al. 2013). The tests entail measuring the serum levels of TSH, T4 and T3 resin uptake (Ackermans et al. 2012). Normal ranges of serum TSH are 0.5-6 uU/ml (Ackermans et al. 2012). Normal ranges for serum T4 and T3 are 4.6-12 ug/dl and 80-180 ng/dl respectively (Ackermans et al. 2012). A lower than normal level of serum TSH is indicative of hyperthyroidism while elevated levels of T4 and T3 are indicative of hyperthyroidism (Hoermann et al. 2013). The serum test can also check for the TSI antibody the cause of Graves’ disease. If the serum tests are abnormal, an ultrasound is performed to check for nodules and inflammation in the thyroid (Laurberg et al. 2014). The ultrasound measures the size of the thyroid gland and the masses within it. The ultrasound also tells if the mass within the thyroid is cystic or solid. A thyroid scan is performed to check for thyroid overactivity, or where the iodine is in excess in the thyroid gland (Palacios, Pascual-Corrales & Galofre 2011). A radioactive iodine uptake test can also be performed during the scan which tells whether the entire thyroid gland or just a node of the gland is causing the overactivity (Palacios, Pascual-Corrales & Galofre 2011). If the cause of hyperthyroidism is suspected to be pituitary, a computed tomography (CT) scan or a magnetic resonance imaging (MRI) test is ordered (Lim et al. 2015). e) Treatment options Treatment options for hyperthyroidism include antithyroid drugs (ATDs) including methimazole, propylthiouracil (PTU) and carbimazole (Bartalena et al. 2015). ATDs work by inhibiting the synthesis of the thyroid hormones (Laurberg et al. 2014). Likely side effects of ATDs include rash, itching, fever and hair loss. The dosage and duration of medication depends with age and severity of the condition. ATDs quickly reverse hyperthyroidism but there are also high rates of recurrences (Bartalena et al. 2015). Another option is radioactive iodine which works by shrinking the thyroid (Bartalena et al. 2015). Radioactive iodine destroys the thyroid producing cells and may also destroy the entire thyroid gland. Radioactive iodine is available in the form of a pill taken once and reassessed after six months. Recurrence is rare but most patients usually develop hypopthyroidism a year after hyperthyroid treatment (Bartalena et al. 2015). Side effects of the radioactive iodine treatment include metallic taste in the mouth, swollen salivary glands and nausea. Another treatment option is thyroidectomy or surgery by removal of a portion or the entire thyroid gland (Bartalena et al. 2015). If surgery is chosen as a treatment option, the patient will have to take thyroid hormone supplements to prevent the development of hypothyroidism (Bartalena et al. 2015). Symptoms related with the condition can be managed by use if beta-blockers such as propranolol for palpitations, anxiety, sweating and blood pressure (Laurberg et al. 2014). Conclusion Located in the front on the neck, the thyroid gland is an important organ in cellular functions. The thyroid gland produces two important hormones thyroxine (T4) and triiodotyrosine (T3) which are involved in metabolism, producing energy for a variety of cellular functions including growth and development. Hyperthyroidism occurs when the function of the thyroid stimulating hormone (TSH) is hindered triggering the thyroid gland to produce excessive T4 and T3. Causes of hyperthyroidism include Graves’ disease, toxic adenoma, toxic multinodular goiter, thyroidititis, and excessive iodine intake and pituitary tumors. Graves’ disease is a common cause, and is an autoimmune disorder producing the TSI antibody which suppresses production of TSH leading to failure of the thyroid gland to control the T4 and T3 production. Toxic functioning nodules work autonomously in producing their own thyroid hormones alongside the thyroid gland leading to excess production. The symptoms of hyperthyroidism have been explained. Diagnosis includes physical examination and family history. Thyroid function tests help to diagnose hyperthyroidism by low TSH and elevated T4 and T3. Thyroid ultrasound and scan, MRIs or CT scans can help to evaluate the severity and cause of hyperthyroidism. Antithyroid medications, radioactive iodine and surgery are treatment options sought for hyperthyroidism. References: Ackermans, M, Kettelarij-Haas, Y, Boelen, A, & Endert, E 2012, ‘Determination of thyroid hormones and their metabolites in tissue using SPE UPLC-tandem MS’, Biomedical Chromatography vol. 26, pp. 485-490. 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