Refers to the clinical manifestation of a group of disorders characterized by excess thyroid hormone activity at the tissue level as a consequence of inappropriately high thyroid hormone levels.

Hyperthyroidism is a subset of thyrotoxicosis which is a manifestation of the excess thyroid hormone production and secretion by the thyroid gland.

Hyperthyroidism prevalence is 1.3% in the US and occurs more commonly in women compared with men, 2% versus 0.2%.

Hyperthyroidism increases with age, iodine deficiency and race, with higher rates in whites compared with Hispanics and African-Americans.

Thyrotoxicosis is the result of inappropriate activation of the hypothalamus-pituitary-thyroid axis with increased thyroid hormone production from thyroid follicles or from release or ingestion of preformed thyroid hormone.

In iodine-sufficient areas, the most common cause of thyrotoxicosis is Graves’ disease accounting for 80% of noniatrogenic cases, followed bu modular thyroid disease and thyroiditis.

Nodular thyroid disease accounts for as much as 50% of cases of thyrotoxicosis in iodine-deficient areas and is more common in the elderly.


In the absence of pathopneumonic clinical findings measurement of TSH receptor antibodies provides a 97% sensitivity and 98-99% specificity for Graves’ disease and can be helpful especially in the setting of a nodular goiter.










In the absence of pathopneumonic clinical findings measurement of TSH receptor antibodies provides a 97% sensitivity and 98-99% specificity for Graves’ disease and can be helpful especially in the setting of a nodular goiter.




Normal increased radioactive iodine uptake with diffuse distribution on a scan can also confirm the diagnosis and distinguishes Graves’ disease from other causes of thyrotoxicosis.




Doppler flow sonography with thyroid ultrasound has good accuracy for Graves’ disease diagnosis with a sensitivity of 87% and the specificity of 100%.




Management of Graves’ disease is twofold: symptom control and treatment of the underlying hyperthyroidism.




Beta blockade  is the mainstay of symptom control for the overstimulation of beta-adrenergic receptors.




Propranolol offers additional benefits by decreasing the peripheral conversion of T4 to T3.




In a thyroid storm glucocorticoids are utilized.




Radioactive iodine ablation, anti-thyroid agents, and thyroidectomy are other treatment options for underlying hyperthyroidism .




Radioactive iodine is the preferred first line approach in the US.




Radioactive iodine usage has been decreasing.




Radioactive iodine I 131 is incorporated into thyroid tissue via the sodium-iodine symporter.




The sodium-iodine symporter gene expression is dependent on TSH receptor activation that occurs diffusely in Graves’ disease.




In Graves’ disease radioactive iodine I 131 is incorporated into the entire thyroid gland.




Following radioactive iodine tissue necrosis occurs over 6-18 weeks, resulting in hypothyroidism in 80-90% of patients after a single dose.




A negative pregnancy test is required for all women of childbearing potential before receiving radioactive iodine treatment.




Anti-thyroid drugs inhibit thyroid hormone synthesis by disrupting thyroid peroxidase iodination of tyrosine residues on thyroglobulin.




The iodination of tyrosine residues on thyroglobulin is a critical step in the formation of T3 and T4.




Anti-thyroid agents available are Propylthiouracil and methimazole.




Methimazole is the preferred drug given the concerns about the hepatic toxicity associated with propylthiouracil.




Mild hyperthyroidism with free T4 level 1-1.5 times the upper limit of normal is usually treated with low dose methimazole, 5 to 10 mg a day, and moderate hyperthyroidism with free T4 levels 1.5-2 times the upper limit of normal can be treated starting with 10-20 mg of methimazole, and severe hyperthyroidism with the free T4 level 2 to 3 times the upper limit of normal treated with high dose methimazole 20 to 40 mg daily in divided doses.




Antithyroid  drugs are given usually for 18 months and then withdrawn to determine if remission is present.




The remission rate with anti-thyroid drugs is 30-50%.




The likelihood of remission decreases with: male sex, age less 40 years, previous recurrence of Graves’ disease, cigarette smoking, large goiter, orbit pathology, high ratio of free T3 to free T4, high tide is New York City thyroid antibodies that diagnosis, and the end of the course of anti-thyroid strokes.




In patients taking ATD’s adverse reactions occur in 13% of patients.




If thyroidectomy is a chosen therapy, patients are pre-treated with ATD’s and beta blockers to induce euthyroidism before surgery.




Iodine solutions are taken for 10 days preoperatively to help normalize thyroid hormone levels, decrease thyroid blood vessels, and minimize surgical blood loss.




Prior to thyroidectomy calcium and vitamin D levels are assessed and repleted before surgery to prevent the development of symptomatic postoperative hypocalcemia.




Thyroidectomy is the preferred treatment for thyrotoxicosis when there is symptoms of compression from a large goiter, the presence of suspicious nodules, or moderate to severe and active orbitopathy in patients who cannot tolerate anti-thyroid drugs.




In Graves’ disease there is a diffuse uptake of radioactive iodine throughout the entire thyroid gland.




Thyroid inflammation in subacute thyroiditis releases increased T3 and T4 and causes thyrotoxicosis.




Exaggerated hyperthyroidism may be due to intentional or accidental ingestion of excessive thyroid hormone.




Biotin is frequently utilized in skin, hair, and nail health products and impacts assays by suppressing TSH value and elevating T4, T3, and thyroid related antibodies.




Thyroid studies should be performed after not taking biotin for a minimum of 12 hours and preferably 24 hours.




Hypothyroidism relating to the use of thyroid scan and uptake: simultaneous TSH value as well as appreciation of iodine status is important.




In patients with elevated iodine uptake and normal TSH/T3/T4 concentrations, iodine deficiency should be suspected rather than hypothyroidism.




Iodine  deficient patients residing in iodine sufficient areas, usually have dietary habits that avoid iodine containing products.




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