![]() Usually 10 to 30 millicurie, depending on uptake and the size of the thyroid gland Immediate release: 10 to 40 mg orally every eight hoursĮxtended release: 80 to 160 mg orally once per dayĮxacerbation of congestive heart failure or asthmaĭecreases T 4 to T 3 conversion nonselective beta blockerĥ to 120 mg orally per day (can be given in divided doses)Ĭontraindicated in the first trimester of pregnancyĪgranulocytosis not related to dose liver dysfunction rash, including ANCA-associated vasculitisĭrug of choice in the first trimester of pregnancy carries a higher risk of liver failure than methimazole Selective beta 1 blocker safer than propranolol in asthma or chronic obstructive pulmonary disease once-daily dosing improves compliance Symptoms pathognomonic for Graves disease: exophthalmos, periorbital edema, diplopia, blurred vision, reduced color perception Increased lacrimation, incomplete closure of the eyes when sleeping reported by the patient's partner, photophobia, increased eye sensitivity to wind or smoke, grittiness or sensation of a foreign body or sand in the eyes Weight loss in spite of increased appetite, fever (in thyroid storm)īrisk peripheral reflexes with accelerated relaxation phase and weakness of proximal musclesĪnxiety, rapid and pressured speech, insomnia, psychosis (if hyperthyroidism is severe) Patchy vitiligo can also be observed in Graves disease Symptoms pathognomonic for Graves disease: pretibial myxedema (thyroid dermopathy) and thyroid acropachy (clubbing of fingers and toes accompanied by soft-tissue swelling of the hands and feet) Onycholysis (Plummer nails), patchy or generalized hyperpigmentation (especially of the face and neck) Tachycardia, irregular pulse (in atrial fibrillation), dyspnea, orthopnea and peripheral edema (in heart failure) Palpitations, tachycardia, anxiety, tremor, jitteriness, diaphoresis, heat intolerance, stare, lid lag, hyperdefecation (not diarrhea) Tumor secreting large quantities of TSH, and not responding to thyroxine and triiodothyronine feedback ![]() Tumor produces β-hCG, which stimulates thyroid TSH receptors Metastasis of functional follicular thyroid cancerĮctopic thyroid tissue in ovarian dermoid tumor produces thyroid hormones Surreptitious ingestion of thyroid hormones Painful inflammation of the thyroid gland caused by viral infection, often with fever, triggering a release of preformed thyroid hormones Subacute granulomatous (de Quervain) thyroiditis Variant of painless thyroiditis with the same mechanism, occurring after delivery ![]() High level of β-hCG stimulates TSH receptors Overproduction of thyroid hormones (amiodarone-induced thyrotoxicosis type 1) or release of preformed thyroid hormones (amiodarone-induced thyrotoxicosis type 2, interferon alfa, interleukin-2, or lithium) ![]() Somatic mutation in TSH receptor or Gs alpha gene in a thyroid noduleĮxpansion of clonogenic cells with an activating TSH receptor mutation Painless or transient (silent) thyroiditisĪutoimmune destruction of thyroid tissue leading to a release of preformed thyroid hormones ![]() The choice of treatment depends on the underlying diagnosis, the presence of contraindications to a particular treatment modality, the severity of hyperthyroidism, and the patient's preference.Īutoimmune process in which antibodies stimulate the TSH receptor leading to overproduction of thyroid hormones Radioactive iodine ablation is the most widely used treatment in the United States. Hyperthyroidism caused by overproduction of thyroid hormones can be treated with antithyroid medications (methimazole and propylthiouracil), radioactive iodine ablation of the thyroid gland, or surgical thyroidectomy. The most common cause of an excessive passive release of thyroid hormones is painless (silent) thyroiditis, although its clinical presentation is the same as with other causes. The most common causes of an excessive production of thyroid hormones are Graves disease, toxic multinodular goiter, and toxic adenoma. Hyperthyroidism is an excessive concentration of thyroid hormones in tissues caused by increased synthesis of thyroid hormones, excessive release of preformed thyroid hormones, or an endogenous or exogenous extrathyroidal source. ![]()
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