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Thyroid Hormones and Calcium Metabolism
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Major control of the synthesis and secretion of thyroid hormones is mediated by the hypothalamic–pituitary axis via the release of thyrotropin-releasing hormone (TRH). TRH acts on the anterior pituitary leading to production and secretion of thyroid-stimulating hormone (TSH). TSH, a glycoprotein, promotes the growth of the thyroid gland and secretion of thyroid hormones by stimulating several steps in its synthesis: iodine uptake and oxidation, formation of MIT and DIT, coupling of MIT and DIT to form T3 and T4, endocytosis and proteolysis of thyroglobulin to release T3 and T4 for secretion.
The endocrine system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Hypothyroidism in the adult is referred to as myxoedema. The symptoms and signs of hyperthyroidism are related to a decrease in metabolic activity due to a decrease in thyroid hormone secretion. The commonest cause of hypothyroidism is autoimmune thyroid disease. Patients with hypothyroidism complain of weight gain, tiredness, and dislike of the cold, constipation, menorrhagia, a hoarse voice and difficulties in thinking. They may show thick dry skin and dry hair, with a slow pulse, non-pitting oedema, ataxia, slow reflexes, peripheral neuropathy and a ‘toad like face’. They may develop psychosis and in severe untreated cases, hypothermia and coma can develop. Raised blood cholesterol levels increase the risk of cardiovascular disease. A goitre may be present. The causes are shown in Box 18.4.
Summation of Basic Endocrine Data
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
TSH is a polypeptide glycoprotein produced and released by the anterior pituitary gland. Its function is to produce and release T3 and T4 within the thyroid gland. The thyroid hormones are essential for bodily growth, development, and metabolism. The hypothalamus controls the TSH level through its TRH.
Protective effects of Portulaca oleracea and vitamin E on cardiovascular parameters in rats with subclinical hyperthyroidism
Published in Clinical and Experimental Hypertension, 2022
Mousa- al-Reza Hadjzadeh, Hadi Khodadadi, Farzaneh Sohrabi, Mahdiyeh Hedayati-Moghadam, Atieh Ghorbani, Sara Hosseinian
Thyroid hormones are fundamental regulators of cardiovascular hemodynamics. Clinical manifestations of hyperthyroidism are due to the effects of thyroid hormones on the cardiovascular system and hemodynamic changes (1). Subclinical hyperthyroidism (SHT) is seen in 0 · 6–16% of the population and is associated with decreased or suppressed TSH levels while the concentration of free T4 is within the normal range (2). SHT can induce significant abnormalities in heart structure and function and causes problems such as increased heart rate, increased incidence of supraventricular arrhythmias, and higher LV mass (3). SHT also impacts on cardiac hemodynamics by affecting left ventricular diastolic function. In addition, SHT causes left ventricular hypertrophy, which is associated with increased risk of cardiovascular disease (2).
Low awareness and under-diagnosis of hypothyroidism
Published in Current Medical Research and Opinion, 2022
Ulrike Gottwald-Hostalek, Barbara Schulte
Subclinical hypothyroidism has been proposed as a modifiable risk factor for adverse cardiovascular outcomes, which may increase the urgency of diagnosing the condition7,41–43. A recent report found that cardiovascular disease mediated about one-seventh of the excess mortality associated with subclinical hypothyroidism9. The relationship between subclinical hypothyroidism and outcome is probably complex however, and likely influenced by multiple factors including age, the severity and duration of exposure to abnormal thyroid hormone levels and, especially, obesity38. Increased psychological stress has been proposed recently as an additional factor other that hypothyroidism that can result in modestly increased TSH levels, and which may also contribute to observations of increased cardiovascular risk associated with TSH in the high-normal range39.
Toward a science-based testing strategy to identify maternal thyroid hormone imbalance and neurodevelopmental effects in the progeny – part I: which parameters from human studies are most relevant for toxicological assessments?
Published in Critical Reviews in Toxicology, 2020
Ursula G. Sauer, Alex Asiimwe, Philip A. Botham, Alex Charlton, Nina Hallmark, Sylvia Jacobi, Sue Marty, Stephanie Melching-Kollmuss, Joana A. Palha, Volker Strauss, Bennard van Ravenzwaay, Gerard Swaen
The thyroid gland is an endocrine organ present in all vertebrates. Thyroxine (T4) is the main thyroid hormone synthesised and secreted by the thyroid, whereas triiodothyronine (T3), the biologically active hormone, is mostly produced by deiodination of T4 in peripheral tissues. A major role of the thyroid hormones is to regulate metabolism, e.g. during growth and reproduction. In developing offspring, rodent data (with supporting evidence in humans) indicate that thyroid hormones play a role in neuronal migration, cellular differentiation (e.g. of neurons) and glial myelination. The thyroid gland is controlled by the pituitary [through secretion of thyroid stimulating hormone (TSH)] which, in turn, is regulated by the thyrotropin releasing hormone secreted by the hypothalamus (Dickhoff and Darling 1983; DeGroot and Jameson 2001). Thyroid hormones are highly hydrophobic and therefore generally bound to serum binding proteins when circulating in the bloodstream, whereas only a minor fraction (<1%) remains as free hormones (e.g. free T4 (fT4) and free T3). It is the free hormone fraction that is sensed by the tissues, triggering the homeostatic regulatory mechanisms (Stockigt 2001).