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Adenoma, toxic

Fuhrer D, Krohn K, Paschke R (2005) Toxic Adenoma and toxic Multinodular Goiter. In Braverman, LE Utiger (Hrsg.) RD (eds) Lippincott Williams Wilkins, ISBN 0-7817-5047-4, The Thyroid, 508-518... [Pg.192]

Hyperthyroidism (thyrotoxicosis), defined as excessive thyroid activity, causes a state of thyroid hormone excess (thyrotoxicosis) characterized by an increased metabolic rate, increase in body temperature, sweating, tachycardia, tremor, nervousness, increased appetite and loss of weight. Common causes of hyperthyroidism are toxic multinodular goiter, toxic adenoma or diffuse toxic goitre ( Graves disease). Antithyroid diugs (methimazol, carbimazole, propylthiouracil) block thyroid hormone production and are hence suitable for the treatment of hyperthyroidism. [Pg.608]

Toxic adenoma Thyroid cancer Struma ovarii... [Pg.676]

An autonomous thyroid nodule (toxic adenoma) is a discrete thyroid mass whose function is independent of pituitary control. Hyperthyroidism usually occurs with larger nodules (i.e., those greater than 3 cm in diameter). [Pg.241]

Toxic adenomas may result in hyperthyroidism with larger nodules. Because there may be isolated elevation of serum T3 with autonomously functioning nodules, a T3 level must be measured to rule out T3 toxicosis if the T4 level is normal. After a radioiodine scan demonstrates that the toxic thyroid adenoma collects more radioiodine than the surrounding tissue, independent function is documented by failure of the autonomous nodule to decrease its iodine uptake during exogenous T3 administration. [Pg.243]

The manifestations of hyperthyroidism depend on the severity of the disease, the age of the patient, the presence or absence of extrathyroidal manifestations, and the specific disorder producing the thyrotoxicosis. Of the various types of hyperthyroidism, only two are common Graves disease and toxic multinodular goiter. Less common causes include toxic adenoma and postpartum thyroiditis, among others. [Pg.749]

Thyroid disorders. Disturbances in thyroid metabolism can occur at any level of the hypothalams-pituitary-thyroid-peripheral tissue axis. Several of these disorders have been discussed previously. Hyperthyroidism is more prevalent in women than men. The three most common causes of hyperthyroidism are Graves hyperthyroidism, toxic multinodular goiter, and toxic adenoma. The clinical features of hyperthyroidism include hyperkinesis, weight loss, cardiac anomalies (e.g., atrial fibrillation), fatigue, weakness, sweating, palpitations, and nervousness. The typical biochemical laboratory parameters are increased serum free T4 and decreased serum TSH. [Pg.778]

Siegel RD, Lee SL. Toxic nodular goiter. Toxic adenoma and toxic multinodular goiter. Endocrinol Metab CUn North Am 1998 27 151-168. [Pg.1388]

Method Toxic adenoma goiter Toxic diffuse goiter Thyroiditis Graves disease... [Pg.790]

Functionally, the state may be compensated up to a certain degree of iodine deficiency and for a considerable period of time, described in clinical terms as euthyroid diffuse or nodular goiter. Functional failure follows only in the presence of severe iodine deficiency, and hypothyroidism may then develop. Much more frequently and somewhat paradoxically, hyperthyroidism ensues after many years of iodine depletion. Rarely, hyperthyroidism may be found in cases of diffuse goiter, which are then termed as diffuse thyroid autonomy. Fiowever, hyperthyroidism frequendy occurs in conjunction with uninodular (toxic adenoma) and multinodular goiters (toxic multinodular goiter). [Pg.790]

Treatment of Toxic Adenoma and Toxic Multinodular Goiter... [Pg.790]

The treatment aims to correct the symptoms experienced by the patient due to the presence of a toxic adenoma or toxic multinodular goiter. There are two types of symptoms functional ones, which relate to hyperthyroidism and mechanical ones, which are due to the pressure exerted by the goiter or nodule, irrespective of the functional impairment caused. [Pg.790]

The treatment of hyperthyroidism requires differentiation between the various types of hyperthyroidism (Table 81.1). Toxic adenoma and toxic multinodular goiter are the most common causes of hyperthyroidism in iodine-deficient countries, as opposed to Graves disease, which is... [Pg.790]

The presence of overt or subcUnical hyperthyroidism indicates the need for treatment of a patient with toxic adenoma, toxic... [Pg.791]

Patients with toxic adenoma or toxic multinodular goiter, in the absence of symptoms and with TSH well in the euthyroid range, may be monitored without therapy. The therapy can frequently be postponed for many years to a later stage. [Pg.791]

Once the diagnosis and indication for treatment have been established, there are three main options for treating patients with toxic adenoma or toxic multinodular goiter ... [Pg.791]

The main use of antithyroid drugs in toxic adenoma and toxic multinodular goiter is therefore to attain a euthyroid state before the patient may undergo other modes of therapy. Another use is to block iodine uptake prior to the exposure to radiographic contrast agents in patients at risk of iodine-induced hyperthyroidism. [Pg.792]

Combination with levothyroxine, a common practice in treating Graves disease, is prohibited in toxic adenoma and toxic multinodular goiter. [Pg.792]

The ideal patient for application of radioactive iodine is therefore one who harbors a single toxic adenoma and shows a suppressed TSH (Table 81.3). Under these conditions, the surrounding healthy thyroid tissue is least affected and the patient leaves the therapy with a high chance of eliminating the overactive hyperfunctioning nodule and, at the same time, preserving the healthy tissue to resume normal thyroid function (Diedein et ai, 2004 Huysmans et aL, 1997 Reiners and Schneider, 2002 Sarkar, 2006). [Pg.792]


See other pages where Adenoma, toxic is mentioned: [Pg.337]    [Pg.759]    [Pg.749]    [Pg.868]    [Pg.899]    [Pg.264]    [Pg.1372]    [Pg.1374]    [Pg.1374]    [Pg.1374]    [Pg.230]    [Pg.232]    [Pg.148]    [Pg.324]    [Pg.450]    [Pg.789]    [Pg.790]    [Pg.790]    [Pg.791]    [Pg.791]    [Pg.791]    [Pg.791]    [Pg.791]    [Pg.792]   
See also in sourсe #XX -- [ Pg.778 ]

See also in sourсe #XX -- [ Pg.921 ]




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