Hyperthyroidism

Directly interferes with thyroid hormone synthesis in the thyroid gland by inhibiting iodide incorporation into thyroglobulin. Iodination of thyroglobulin is an important step in synthesizing the thyroid hormones thyroxine (T4) and triiodothyronine (T3). Eventually, thyroglobulin is depleted and the circulating thyroid hormone level drops (Jones and Bartlett Learning, 2018).

Thyrotoxicosis is a condition that results from any cause of increased amounts of thyroid hormone (TH) levels. Hyperthyroidism is a form of thyrotoxicosis in which excess amounts of TH are secreted from the thyroid gland. (Brasher, Jones, and Huether, 2018). The thyroid contributes to the body’s energy output by regulation of cardiac rate and output, lipid catabolism, heat production, and skeletal growth, which explains the wide range of symptoms related to thyroid abnormalities(Petrulea, Muresan, & Duncea, 2012).

TSI's override the normal negative feedback mechanism. The TSI stimulation of the TSH receptors in the thyroid gland results in hyperplasia of the gland, known as a goiter (Brashers, Jones, & Huether, 2018).

A major threat to homeostasis and therefore to the integrity of aerobic organisms arises from chemical species possessing one or more unpaired electrons in their outer orbital, called free radicals.(Petrulea, Muresan, & Duncea, 2012).

Thyroid hormones affect cell metabolism by altering protein, fat, and glucose metabolism and, as a result, heat production and oxygen consumption are increased. (Brashers, Jones, & Huether, 2018)

Thyroid hormones work on many Thyroid Response Elements (areas that affect the transcription of DNA within the cells), includingalpha myosin heavy chain fusion (MHC-α)sarcoplasmic reticulum calcium-activated ATPase (SERCA)cellular membrane Na-K pump (Na-K ATPase)β1 adrenergic receptorcardiac troponin Iatrial natriuretic peptide (ANP) (Ertek & Cicero, 2013)

Triiodothyronine (T3) is formed from coupling monoiodotyrosine (one iodine atom and tyrosine) and diiodotyrosine (two iodine atoms and tyrosine). (Brashers, Jones, & Huether, 2018)

Thyroxine (T4) is formed by coupling two diiodotyrosines. (Brashers, Jones, & Huether, 2018)

Glycoprotein hormone that is synthesized and stored in the anterior pituitary gland. The primary effects of TSH include: An immediate increase in the release of stored Thyroid hormone (TH) An increase in the iodine uptake and oxidation An increase in thyroid hormone synthesis An increase in the synthesis and secretion of prostaglandins by the thyroid (Brashers, Jones, & Huether, 2018)

For this test, you take a small, oral dose of radioactive iodine. Over time, the iodine collects in your thyroid gland because your thyroid uses iodine to manufacture hormones. You'll be checked after two, six or 24 hours — and sometimes after all three time periods — to determine how much iodine your thyroid gland has absorbed.A high uptake of radioiodine indicates your thyroid gland is producing too much thyroxine. The most likely cause is either Graves' disease or hyperfunctioning nodules (Mayo Clinic, 2018).

TSI's contribute to the two major distinguishing manifestations of Graves disease: ophthalmopathy and dermopathy. Exophthalmos (protrusion of the eyeball) is caused by an increased secretion of hyaluronic acid, adipogenesis, inflammation, and edema of the orbital contents (Brashers, Jones, & Huether, 2018).

The strong inotropic activity of thyroid hormones is probably due to an increased number of β-adrenergic receptors(Ertek & Cicero, 2013).

Since the first descriptions of hyperthyroidism and thyrotoxicosis, the cardiovascular symptoms have been alarming signs for the physician in the clinical presentation of the patient. Palpitations, exercise intolerance, dyspnea, angina-like chest pain, peripheral edema and congestive heart failure are common symptoms of hyperthyroidism (Ertek and Cicero, 2013).

References:Brashers, V. L., Jones, R. E., & Huether, S. E. (2018). Alterations in Hormonal Regulation. In K. L. McCance, & S. E. Huether, Pathophysiology. The Biological Basis for Disease in Adults and Children (pp. 669-712). St. Louis: Elsevier.Ertek, S., & Cicero, A. F. (2013). Hyperthyroidism and cardiovascular complications: a narrative review on the basis of pathophysiology. Archives of Medical Science, 9, 944-952.Jones and Bartlett Learning. (2018). 2018 Nurse's Drug Handbook. Burlington: Jones and Bartlett Learning.Mayo Clinic. (2018). Hyperthyroidism. Retrieved from Patient Care and Health Information: https://www.mayoclinic.org/diseases-conditions/hyperthyroidism/diagnosis-treatment/drc-20373665Petrulea, M., Muresan, A., & Duncea, I. (2012). Oxidative Stress and Antioxidant Status in Hypo- and Hyperthyroidism. Antioxidant Enzyme. Retrieved from https://www.intechopen.com/books/antioxidant-enzyme/oxidative-stress-and-antioxidant-status-in-hypo-and-hyperthyroidism