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Hyperthyroidism antithyroid drugs

Pretreatment with antithyroid drugs is necessary to avoid the risk of thyroid storm (exacerbation of hyperthyroidism with fever and tachycardia) in the following groups the elderly, people with cardiac disease, and people with severe hyperthyroidism. Antithyroid drugs should be stopped at least 4 days before radioactive iodine is given, and restarted no sooner than 3 days after, to permit uptake of the iodine into the thyroid gland. Antithyroid drugs can usually be stopped after 2-6 weeks as the radioactive iodine takes effect. [Pg.761]

Antithyroid drugp or thyroid antagonists are used to treat hyperthyroidism. In addition to the antithyroid drugs, hyperthyroidism may be treated by the administration of strong iodine solutions, use of radioactive iodine (131I), or by surgical removal of some or almost all of the tiiyroid gland (subtotal thyroidectomy). [Pg.534]

Before a patient starts therapy with an antithyroid drug, die nurse obtains a history of the symptoms of hyperthyroidism. It is important to include vital signs, weight, and a notation regarding the outward symptoms of die hyperthyroidism (see Table 51-1) in the physical assessment. If die patient is prescribed an iodine solution, it is essential that die nurse take a careful allergy history, particularly to iodine or seafood (which contains iodine). [Pg.535]

The patient with hyperthyroidism is likely to have cardiac symptoms such as tachycardia or palpitations. Propranolol, a adrenergic blocking drug (see Chap. 21), may be prescribed by tlie primary health care provider as adjunctive treatment for several weeks until tlie therapeutic effects of tlie antithyroid drug are obtained. [Pg.536]

Some neonates born to mothers with Graves disease will be hyperthyroid at delivery. Antithyroid drug therapy (propylthiouracil 5-10 mg/kg per day or methimazole 0.5-1 mg/kg per day) may be required for up to 12 weeks. One drop per day of SSKI may be used in the first few days to rapidly reduce thyroid hormone synthesis and release. [Pg.680]

In the hyperthyroid patient, relieving signs and symptoms and achieving a euthyroid state are the desired outcomes. The method of achieving these outcomes may change over time with the use of antithyroid drugs versus radioactive iodine. [Pg.682]

Blockers are usually used as adjunctive therapy with antithyroid drugs, RAI, or iodides when treating Graves disease or toxic nodules in preparation for surgery or in thyroid storm. /3-Blockers are primary therapy only for thyroiditis and iodine-induced hyperthyroidism. [Pg.245]

Antithyroid drugs are not routinely used after RAI because their use is associated with a higher incidence of posttreatment recurrence or persistent hyperthyroidism. [Pg.246]

Carbimazole is an antithyroid drug indicated in hyperthyroidism. It is usually administered as 15 mg daily in the morning. Carbimazole tends to cause agranulocytosis and therefore patients are advised to report immediately any signs of infections, such as sore throat. [Pg.291]

The 3-blockers significantly reduce the peripheral manifestations of hyperthyroidism, particularly elevated heart rate, increased cardiac output, and muscle tremors. Although the 3-blockers can improve the clinical status of the hyperthyroid patient, the patient remains biochemically hyperthyroid. The 3-blockers should not be used as the sole form of therapy in hyperthyroidism. They are most logically employed in the management of hyperthyroid crisis, in the preoperative preparation for thyroidectomy, and during the initial period of administration of specific antithyroid drugs (see Chapter 65). [Pg.115]

In addition, the metabohsm of OCAs results in the release of large amounts of E into the circulation. As described for KI, I released from OCAs may have effects at the thyroid gland and if used alone to treat hyperthyroidism, OCAs carry the same potential to induce increased secretion of thyroid hormone and exacerbation of thyrotoxicosis. When an OCA is used in the treatment of hyperthyroidism, large doses of antithyroid agents are usually administered concomitantly. However, the combination of OCAs and antithyroid drugs may cause resistance to the antithyroid drugs with time, presumably because of the elevation in intrathyroidal 1 content. Thus, it is recommended that the use of OCAs be reserved for short-term treatment of patients with severe thyrotoxicosis and significant comorbidity (e.g., myocardial infarction, sepsis, stroke) for rapid control of plasma Tj concentrations. [Pg.751]

The three primary methods for controlling hyperthyroidism are antithyroid drug therapy, surgical thyroidectomy, and destruction of the gland with radioactive iodine. [Pg.867]

Antithyroid drugs may also suppress lymphocytic infiltration into the thyroid and thereby directly modulate the basic disorder of autoimmune hyperthyroidism (SEDA-6, 364 SEDA-9, 344). Propylthiouracil, but not the thioimidazoles, also inhibits the conversion of thyroxine to its more active derivative triiodothyronine. This effect is significant during high-dose treatment, and propylthiouracil may therefore be preferred if a more rapid onset of action is desired, for example thyrotoxic crisis, although clear experimental proof of the advantageous effect is still lacking (3). [Pg.335]

The long-term effects of antithyroid drug treatment on the prevalence of ANCAs has been examined in 209 consecutive patients with hyperthyroidism who had been treated with antithyroid drugs, radioactive iodine, thyroidectomy, or a combination of these treatment options... [Pg.339]

Neonatal hypothyroidism has been reported after maternal use of antithyroid drugs (106,107). Transient neonatal hyperthyroidism in a female child born to a mother who had been treated with potassium iodide and carbimazole during pregnancy was followed by sexual precocity (108). [Pg.342]

Stege R. Antithyroid drug therapy in hyperthyroidism. Recurrence, hypothyroidism and thyroid antibodies. Acta Chir Scand Suppl 1980 501 1-130. [Pg.342]

Slot MC, Links TP, Stegeman CA, Tervaert JW. Occurrence of antineutrophil cytoplasmic antibodies and associated vasculitis in patients with hyperthyroidism treated with antithyroid drugs a long-term followup study. Arthritis Rheum 2005 53(1) 108-13. [Pg.344]

Color-flow Doppler sonography can be of use in distinguishing the two types, because type 1 is associated with increased vascularity and type 2 is not. In a retrospective study of 24 patients with amiodarone-induced hyperthyroidism in an iodine-replete environment, 13 had little or no vascularity, of whom seven were prednisolone-responsive of 11 patients with increased vascularity, four responded to antithyroid drugs alone and only one of seven responded to prednisolone (37). Euthyroidism was achieved twice as rapidly in patients with low vascularity than in those with increased vascularity. Thus, responsiveness to prednisolone was not consistently predicted by lack of vascularity, but the presence of flow appeared to correlate with non-responsiveness to prednisolone. [Pg.575]

A 40 year-old patient with severe amiodarone-induced hyperthyroidism after heart transplantation did not respond to high doses of antithyroid drugs combined with glucocorticoids (62). A low dose of lithium carbonate resulted in normalization of thyroid function. [Pg.577]

Although iodide is effective in treating hyperthyroidism for short periods, the effects of this drug begin to diminish after about 2 weeks of administration.35 Consequently, iodide is used in limited situations, such as temporary control of hyperthyroidism prior to thyroidectomy. In addition, iodide may cause a severe hypersensitive reaction in susceptible individuals. Therefore, the use of iodide has been replaced somewhat by other agents such as antithyroid drugs and beta blockers. [Pg.463]

Excessive catecholamine action is an important aspect of the pathophysiology of hyperthyroidism, especially in relation to the heart (see Chapter 38 Thyroid Antithyroid Drugs). The Bantagonists have salutary effects in this condition. These beneficial effects presumably relate to blockade of adrenoceptors and perhaps in part to the inhibition of peripheral conversion of thyroxine to triiodothyronine. The latter action may vary from one Bantagonist to another. Propranolol has been used extensively in patients with thyroid storm (severe hyperthyroidism) it is used cautiously in patients with this condition to control supraventricular tachycardias that often precipitate heart failure. [Pg.220]

Q8 The drug treatment of thyrotoxicosis involves using antithyroid drugs car-bimazole (which is converted to the active compound methimazole) and propylthiouracil inhibit the synthesis of thyroid hormone. Propylthiouracil also inhibits peripheral conversion of T4 to T3. Many of the symptoms of hyperthyroidism can also be alleviated by fl-adrenoceptor antagonists. Iodine... [Pg.144]

Graves hyperthyroidism in the United States is treated in most adults (69%) with whereas the remaining patients receive treatment with the antithyroid drugs PTU or MMI. Conversely, antithyroid drugs are used in Europe (77%) and Japan (88%) in most Graves disease patients, whereas the rest are treated with RAI. [Pg.653]


See other pages where Hyperthyroidism antithyroid drugs is mentioned: [Pg.680]    [Pg.680]    [Pg.257]    [Pg.378]    [Pg.246]    [Pg.246]    [Pg.762]    [Pg.750]    [Pg.248]    [Pg.317]    [Pg.324]    [Pg.337]    [Pg.342]    [Pg.350]    [Pg.575]    [Pg.403]    [Pg.463]    [Pg.471]    [Pg.410]    [Pg.242]    [Pg.243]    [Pg.652]    [Pg.653]   
See also in sourсe #XX -- [ Pg.678 , Pg.679 ]




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