This antibody mimics the function of normal thyroid-stimulating hormone. It attaches to the surface of thyroid cells and turns on the cells to produce thyroid hormones, leading to overproduction of these hormones overactive thyroid. The Tg gene produces thyroglobulin a protein that is found only in thyroid tissue and plays a role in the production of thyroid hormones. The TSHR gene produces a protein that is a receptor and binds to thyroid stimulating hormone. The disorder usually develops during middle age with a peak incidence of , but can also affect children, adolescents and the elderly. Some relatives may have had hyperthyroidism or an underactive thyroid; others may have other autoimmune diseases including premature graying of the hair beginning in their 20s.
Similarly, there may be a history of related immune problems in the family, including juvenile diabetes, pernicious anemia due to lack of vitamin B12 or painless white patches on the skin known as vitiligo. It is characterized by an enlarged thyroid gland that is infiltrated with lymphocytes.
Eventually, the thyroid may be completely destroyed. Treatment consists of replacing the amount of hormone that your own thyroid can no longer make with L-thyroxine, the synthetic form of the major thyroid hormone produced by the thyroid gland. Other causes of hyperthyroidism include a toxic nodular or multinodular goiter, which is characterized by one or more nodules or lumps in the thyroid that gradually grow and increase their activity so that the total output of thyroid hormone into the blood is greater than normal.
Also, people may temporarily have symptoms of hyperthyroidism if they have a condition called thyroiditis. This condition is caused by a problem with the immune system or a viral infection that causes the gland to leak stored thyroid hormone.
Types of thyroiditis include subacute thyroiditis, silent thyroiditis, infectious thyroiditis, radiation-induced thyroiditis and postpartum thyroiditis. Most of the time, the thyroiditis resolves. Finally, hyperthyroid symptoms can also be caused by taking too much thyroid hormone in tablet form.
The specific form of treatment recommended may be based upon the age of an affected individual and the degree of the illness. These drugs are especially preferred for the treatment of young children and pregnant women, individuals with mild cases of hyperthyroidism, or individuals in whom prompt control of hyperthyroidism is required. Iodine is a chemical element used by the thyroid gland to create synthesize thyroid hormones. Affected individuals will swallow a solution containing radioactive iodine, which will travel through the bloodstream and collect in the thyroid gland where it will damage and destroy thyroid tissue.
This will shrink the thyroid and reduce the overproduction thyroid hormones. If thyroid hormone levels fall too low, hormone therapy to regain adequate levels of thyroid hormone may be necessary.
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The other definitive therapy is surgery to remove all or part of the thyroid gland thyroidectomy. Hypothyroidism is common after surgery; indeed, this may be the desired outcome. In addition to the three above-mentioned treatments, drugs that block thyroid hormone that is already circulating in the blood from performing its functions beta blockers may be prescribed.
Beta blockers such as propranolol, atenolol, or metoprolol can be used. When thyroid hormone levels return to normal, therapy with beta blockers can be stopped. Lifelong follow up and laboratory studies are necessary in many cases. In some cases, lifelong hormone replacement therapy may be necessary.
Orbital decompression surgery and orbital radiotherapy may also be necessary in more severe cases. During orbital decompression surgery, a surgeon takes out the bone between the eye socket orbit and the sinuses. This allows the eye to fall back into its natural position within the eye socket. This surgery is generally reserved for individuals who are at risk of vision loss due to pressure on the optic nerve or in whom other treatment options have not worked.
Information on current clinical trials is posted on the Internet at www. All studies receiving U. For information about clinical trials sponsored by private sources, contact: www. Immunogenetics of autoimmune thyroid diseases: a comprehensive review.
Symptoms of hyperthyroidism
J Autoimmun. Tomer Y. Mechanisms of autoimmune thyroid diseases: from genetic to epigenetics. Annu Rev Pathol. Rivkees SA. Int J Pediatr Endocrinol.
Thyroid disease - Wikipedia
Bartalena L, Fatourechi V. J Endocrinol Invest. We have a dedicated site for Germany. Both thyroid dysfunction and heart failure show a high prevalence in the adult population. Frequently, in clinical practice, a multidisciplinary approach is useful to optimize the management of patients with these conditions. Although there is no doubt regarding the close link between cardiovascular pathophysiology and thyroid homeostasis, our understanding of this association is far from being exhaustive.
Thyroid hormone regulates the expression of cardiac-specific functional contractile and structural proteins and plays a pivotal role in modulating both diastolic and systolic function as well as peripheral vascular resistance. The close relationship between thyroid and heart dysfunction is strongly supported by recent evidence demonstrating that an altered thyroid profile is a negative prognostic predictor in patients with heart failure. The treatment of chronic heart failure, especially in advanced stages of the disease, continues to be an open and challenging field.
The potential of novel thyroid hormone therapies that address the molecular biology of thyroid dysfunction and heart failure thus represents an attractive area of multidisciplinary scientific interest. This book is a readable, integrated, and highly up to date presentation of the clinical, pathophysiological, and basic science aspects of thyroid—heart failure interactions. It addresses a complex subject in an approach that targets a large audience of readers. This book attempts to gather the most up-to-date information about the pathophysiological and clinical significance of thyroid disease in relationship to heart failure.