However, in some cases, you may be referred immediately to a doctor who specializes in the body's hormone-secreting glands endocrinologist. If you have eye involvement, you may also be referred to an eye doctor ophthalmologist. It's good to prepare for your appointment. Here's some information to help you get ready for your appointment, and to know what to expect from your doctor. Preparing a list of questions will help you make the most of your time with your doctor.
For hyperthyroidism, some basic questions to ask your doctor include:. Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission. This content does not have an English version. This content does not have an Arabic version. Diagnosis Hyperthyroidism is diagnosed using: Medical history and physical exam. During the exam your doctor may try to detect a slight tremor in your fingers when they're extended, overactive reflexes, eye changes and warm, moist skin.
Your doctor will also examine your thyroid gland as you swallow to see if it's enlarged, bumpy or tender and check your pulse to see if it's rapid or irregular. More Information Thyroidectomy. Request an Appointment at Mayo Clinic. Share on: Facebook Twitter. Show references AskMayoExpert.
Rochester, Minn. De Leo S, et al. The Lancet. Merck Manual Professional Version. Accessed Oct. American Thyroid Association. Hyperthyroidism overactive thyroid. Burch HB, et al. Management of Graves disease. Graves' disease. Podrid PJ.
Major side effects of beta blockers. Davies TF, et al. It is contraindicated in pregnancy. Moderate to severe Graves orbitopathy is a relative contraindication, especially in patients who smoke, because radioactive iodine may exacerbate the eye disease. Nonradioactive iodine impedes radioactive iodine uptake by iodide transporter; therefore, exposure to large amounts of nonradioactive iodine e.
Pregnancy should be ruled out within 48 hours before radioactive iodine ablation and avoided for six months thereafter.
Most patients develop permanent hypothyroidism between two and six months after radioactive iodine ablation and require thyroid hormone supplementation. This treatment option is preferred in patients with goiter-induced compressive symptoms and in patients with contraindications to radioactive iodine ablation or thionamides. Besides general anesthesia risk, thyroidectomy carries a risk of inadvertently injuring parathyroid glands and recurrent laryngeal nerves.
Antithyroid medications can control hyperthyroidism, but do not induce remission of hyperthyroidism associated with toxic adenoma or toxic multinodular goiter. Therefore, radioactive iodine ablation and thyroidectomy are the main treatment options for these conditions. Thyroidectomy is favored if a nodule or goiter causes compressive symptoms. Antithyroid medications may be used for long-term treatment in select patients who refuse ablation or who have a contraindication to thyroidectomy.
Painless thyroiditis and subacute thyroiditis are self-limiting conditions that usually resolve spontaneously within six months. There is no role for antithyroid medications or radioactive iodine ablation in the treatment of thyroiditis. Beta blockers may be used if needed to control adrenergic symptoms. Pain associated with subacute thyroiditis may be relieved with a nonsteroidal anti-inflammatory drug. Graves disease, toxic adenoma, and toxic multinodular goiter can sometimes cause severe hyperthyroidism, which is termed a thyroid storm.
The Burch-Wartofsky score is a helpful tool for diagnosing thyroid storm 37 eTable B. Treatment of thyroid storm is summarized in eTable C. Extreme lethargy. Gastrointestinal-hepatic dysfunction. Abdominal pain. Unexplained jaundice. Cardiovascular dysfunction. Tachycardia bpm. Pedal edema. Bibasilar rales. Pulmonary edema.
Atrial fibrillation. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin North Am. Airway maintenance. IV fluids. Cooling blanket do not use salicylate to treat fever because salicylates increase free T 4 and free T 3 levels.
Methimazole Tapazole orally, rectally, via nasogastric tube, or IV, 20 to 40 mg every eight hours. Propylthiouracil orally, rectally, or via nasogastric tube, to mg every eight hours. Saturated solution of potassium iodide, five drops orally every six hours to be started at least one hour after administration of an antithyroid agent.
Esmolol Brevibloc IV, 50 to mcg per kg per minute. Propranolol, 60 to 80 mg orally every four hours. Metoprolol IV, 5 to 10 mg every two to four hours. If beta-blockade is contraindicated, use diltiazem IV, 0. Hydrocortisone mg IV every eight hours also suppresses autoimmune process in Graves disease. Information from Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Amiodarone-induced thyrotoxicosis can be classified as type 1 thyroid hormone overproduction, treated with antithyroid medications or type 2 thyroid tissue destruction, treated with steroids.
Amiodarone should not be discontinued unless it can be stopped safely, without triggering cardiac complications. Hyperthyroidism associated with use of other medications e. The physician should determine whether the medication may be discontinued safely or replaced with a different medication. Data Sources : A PubMed search was performed in Clinical Queries using the key terms hyperthyroidism, thyrotoxicosis, Graves disease, toxic multinodular goiter, toxic adenoma, and thyroiditis.
The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Search dates: December 26, , and August 24, The author thanks Dr. Harold E. Carlson and Dr. Marie C. Gelato for reviewing this manuscript. Already a member or subscriber? Log in. Interested in AAFP membership? Learn more. Reprints are not available from the author.
Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists [published corrections appear in Thyroid.
Vanderpump MP. The epidemiology of thyroid disease. Br Med Bull. Sibling recurrence risk in autoimmune thyroid disease. Genetics and phenomics of inherited and sporadic non-autoimmune hyperthyroidism. Mol Cell Endocrinol. Thyroiditis [published correction appears in N Engl J Med. N Engl J Med. Incidence rate of symptomatic painless thyroiditis presenting with thyrotoxicosis in Denmark as evaluated by consecutive thyroid scintigraphies.
Scand J Clin Lab Invest. Thyroiditis: an integrated approach. Am Fam Physician. Thyroid disease in pregnancy [published correction appears in Am Fam Physician. Clinical and molecular features of a TSH-secreting pituitary microadenoma. Thyroid-adrenergic interactions: physiological and clinical implications. Neuromuscular findings in thyroid dysfunction: a prospective clinical and electrodiagnostic study. J Neurol Neurosurg Psychiatry. Depression, anxiety, health-related quality of life, and disability in patients with overt and subclinical thyroid dysfunction.
Arch Med Res. The spectrum of thyroid disease and risk of new onset atrial fibrillation: a large population cohort study. J N, Francis J. Atrial fibrillation and hyperthyroidism. Indian Pacing Electrophysiol J.
Incidence, clinical characteristics and outcome of congestive heart failure as the initial presentation in patients with primary hyperthyroidism. Bartalena L, Fatourechi V. Extrathyroidal manifestations of Graves' disease: a update. J Endocrinol Invest. Relationship between cigarette smoking and Graves' ophthalmopathy. Fatourechi V. Pretibial myxedema: pathophysiology and treatment options. Am J Clin Dermatol. Thyroid dermopathy and acropachy.
Inverse log-linear relationship between thyroid-stimulating hormone and free thyroxine measured by direct analog immunoassay and tandem mass spectrometry. Clin Chem.
Dufour DR. Laboratory tests of thyroid function: uses and limitations. Beck-Peccoz P, Persani L. TSH-induced hyperthyroidism caused by a pituitary tumor. Nat Clin Pract Endocrinol Metab. Philadelphia, Pa. Antithyroid drug regimen for treating Graves' hyperthyroidism. Cochrane Database Syst Rev. A second course of antithyroid drug therapy for recurrent Graves' disease: an experience in endocrine practice. Antithyroid drug-induced agranulocytosis: report of 13 cases. Chang Gung Med J. Antithyroid drug-related hepatotoxicity in hyperthyroidism patients: a population-based cohort study.
Br J Clin Pharmacol. Weetman AP. Radioiodine treatment for benign thyroid diseases. Clin Endocrinol Oxf. The surgical management of goiter: Part II. Surgical treatment and results. The thyroid gland is found in the neck. It produces hormones that are released into the bloodstream to control the body's growth and metabolism. These hormones are called thyroxine and triiodothyronine. They affect processes such as heart rate and body temperature, and help convert food into energy to keep the body going.
In hyperthyroidism, the thyroid gland produces too much thyroxine or triiodothyronine, which speeds up the body's metabolism. There are several possible underlying causes, the most common being Graves' disease, in which the body's immune system targets the thyroid gland and causes it to produce too much of the thyroid hormones.
Read more about the causes of an overactive thyroid gland. An overactive thyroid usually responds well to treatment, and most people are able to control their symptoms. Beta-blockers may also sometimes be used to temporarily relieve many symptoms of an overactive thyroid gland, although it doesn't target the thyroid gland itself. It's common for treatment to lead to the thyroid not producing enough hormones. This is known as having an underactive thyroid gland hypothyroidism.
However, an underactive thyroid is not usually serious and is easily treated. Read more about the treatment of an overactive thyroid gland. Around 1 in 20 people with Graves' disease will also develop symptoms affecting their eyes, such as:. This is known as Graves' ophthalmopathy and should be seen by a doctor who specialises in treating eye conditions an ophthalmologist. A rarer and more serious complication is a sudden and severe flare-up of symptoms, known as a thyroid storm.
A thyroid storm can be life-threatening, as it causes severe dehydration and heart problems. Read more about the complications of an overactive thyroid gland. It is estimated that around 1 in 50 women in England currently live with an overactive thyroid gland.
In most cases, symptoms will begin somewhere between the ages of 20 and 40, though they can start at any age, including in childhood.
An overactive thyroid gland occurs most frequently in white and Asian people, and less frequently in African-Caribbean people. An overactive thyroid hyperthyroidism has many signs and symptoms, although it is unlikely you would develop all of them.
If you have diabetes , your diabetic symptoms, such as extreme thirst and tiredness, may be made worse by hyperthyroidism. See your GP if you are experiencing any of the above. They may not be the result of an overactive thyroid gland, but they will need further investigation. It might be useful to make a list of your symptoms, as this can often be helpful in determining the correct diagnosis.
Overactive thyroid hyperthyroidism occurs when your thyroid gland produces too much of the thyroid hormones thyroxine or triiodothyronine. Overproduction of thyroid hormones can be caused by a number of conditions, which are outlined below. Graves' disease is the most common cause of overactive thyroid. It can run in families and can occur at any age, although it is most common in women aged years old.
You are more likely to develop Graves' disease if you smoke. Graves' disease is an autoimmune condition. This means the immune system mistakes something in the body for a toxic substance and attacks it. In Graves' disease, it attacks the thyroid gland, which leads to an overproduction of the thyroid hormones.
It is not known what triggers the immune system to do this. Like many autoimmune conditions, it is thought that a combination of both genetic and environmental factors could be involved.
If you have Graves' disease, your eyes may also be affected, causing discomfort and double vision. This is known as Graves' ophthalmopathy. You may find your eyes bulge out or appear more prominent. For more information on Graves' ophthalmopathy, read our page on complications of an overactive thyroid gland. It is possible for lumps to develop in your thyroid gland.
These are known as nodules. It is not known why nodules develop, but they are usually non-cancerous benign. However, the nodules can contain abnormal thyroid tissue, which affects the normal production of thyroxine or triiodothyronine, causing an overactive thyroid.
Nodules that contain abnormal thyroid tissue are described as toxic. Iodine contained in the food you eat is used by your thyroid gland to produce the thyroid hormones thyroxine and triiodothyronine. However, taking additional iodine in supplements can cause your thyroid gland to produce too much thyroxine or triiodothyronine. This is known as iodine-induced hyperthyroidism — sometimes referred to as Jod-Basedow phenomenon.
It usually only occurs if you already have nodules in your thyroid gland. Amiodarone is a type of medication known as an anti-arrhythmic, which helps to control an irregular heartbeat atrial fibrillation. If you have non-toxic nodules in your thyroid gland, taking amiodarone can cause hyperthyroidism because it contains iodine.
Amiodarone can cause a type of hyperthyroidism usually more severe and difficult to treat through a harmful effect on thyroid tissue. This type of hyperthyroidism is called amiodarone-induced hyperthyroidism. In rare cases, you may develop an overactive thyroid as a result of thyroid cancer that starts in your thyroid follicles.
This can occur if cancer cells in your thyroid gland begin to produce thyroxine or triiodothyronine. This is also known as functioning thyroid cancer.
A diagnosis will be based on your symptoms and the results of blood tests that assess how well your thyroid gland is working. These are known as thyroid function tests. TSH is made in the pituitary gland in your brain and controls the production of thyroxine and triiodothyronine. If you have an overactive thyroid, the thyroid function test will show that levels of TSH in your blood are consistently lower than normal. Low levels of TSH mean your thyroid gland is overactive and likely to be making excessive thyroid hormones.
This is the first part of the thyroid function test. Your GP will then test your blood for levels of thyroxine and triiodothyronine. If you have an overactive thyroid, you will have higher than normal levels of both these hormones. In some cases, tests may show you have normal thyroid hormone levels, but low or suppressed levels of TSH.
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