Definition:
Diagnosis
History and physical.
Labs/studies ordered/reviewed:
-TSH first. If low, then free T4 and T3. CBC, CMP (review calcium level). R/o elevated alkaline phosphatase or hypercalciuria.
–RAIU scan.
-Thyroglobulin if concern for exogenous T4 overdose (it will be low).
-U/S if nodule noted on exam.
Treatment
Beta-blockers to control the adrenergic symptoms. Indicated for pts with CAD and resting pulse > 90 or elderly patients with symptoms of thyrotoxicosis.
Graves disease is treated with 1) antithyroid medication (Methimazole or PTU), 2) Radioactive iodine treatment, 3) Surgery. Glucocorticoids may be used in pts with mod-severe Graves Ophthalmopathy.
-Methimazole 1st line.
-PTU is 1st-line in pregnant women and 2nd line in all others.
-Radioactive iodine (RAI) ablation – outpatient tx by the endocrinologist.
-Refer to endocrinology.
Thyroid storm treatment: Beta-blocker, PTU or Methimazole, iopanoic acid or iodide > 1h after PTU. May use steroids to decrease T4 to T3 conversion.
Thyroidectomy
Beta-blocker choices. Immediate release Propanolol 10 to 40 mg PO q 8h. Extended-release Propanolol: 80 to 160 mg PO once daily. May also use Atenolol 25 to 100 mg PO once daily. NB: Propranolol also decreases the conversion of T4 to T3. It inhibits 5′-monodeiodinase, thus blocking peripheral conversion of T4 to T3.
Note. If a patient with thyrotoxicosis gets amiodarone, they have to wait before doing a RAIU because amiodarone contains iodine and will interfere with the test.
“Unlike radioactive iodine, methimazole has been shown to decrease the risk of development or progression of ophthalmopathy in Graves disease (SOR B). Atenolol is used for symptomatic control in hyperthyroidism. Cholestyramine can help lower thyroid hormone acutely but is not a long-term treatment. Prednisone is used for severe hyperthyroidism and not long-term treatment. Atenolol, cholestyramine, and prednisone do not have any effect on the long-term complications of Graves disease.” ABFM critique
“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. The most common causes of an excessive production of thyroid hormones are Graves disease, toxic multinodular goiter, and toxic adenoma. 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. 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. Radioactive iodine ablation is the most widely used treatment in the United States. 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.” AAFP 2016
“Methimazole and propylthiouracil (PTU) are the two oral antithyroid medications available. However, because of reports of severe hepatocellular damage, methimazole should be used instead of PTU unless it is contraindicated. Radioactive iodine treatment (131I) is an option, especially for patients who do not achieve remission with antithyroid medications. However, worsening of preexisting orbitopathy is a well-recognized potential complication of 131I treatment, as well as a transient increase in thyroid hormone levels that can precipitate thyroid storm. Thus, patients with elevated free T3 or free T4 levels should be treated with methimazole prior to 131I administration. Thyroidectomy is most often recommended for patients with thyroid nodules and those who are suspected of having cancer or who do not tolerate or refuse alternative forms of therapy. However, antithyroid medication should be given to achieve a euthyroid state prior to surgery in most patients.
Ref: McDermott MT: Hyperthyroidism. Ann Intern Med 2012;157(1):ITC1-ITC16.” ABFM
Approach to thyroid disorders by Marc S. Sabatine, Pocket Medicine 4th Edition.
Resources:
-Great article from AFP, 2016. http://www.aafp.org/afp/2016/0301/p363.html
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