Sandbox: hyperthyroidism landing
Template:Hyperthyroidism landing Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]
Overview
Patient information
Overview
Hyperthyroidism is a disorder that the thyroid gland makes too much thyroid hormone. About 1 percent of the U.S. population has hyperthyroidism. Some diseases, such as Graves’ disease, thyroid nodules and thyroiditis, are associated with the cause of hyperthyroidism. Hyperthyroidism can affect your metabolism. Usual signs and symptoms include goiter, increased appetite but weight loss, palpitation, hypertension, increased sensitivity to heat and perspiration, nervousness and hand tremors. The Thyroid-Stimulating Hormone (TSH) test is a very sensitive and useful test to identify the disorder. Other examinations include the T3 and T4 test, radioactive iodine uptake test and thyroid scan. Treatment options of hyperthyroidism depend on the cause, age, physical condition and the severity of symptoms. Usual treatment measures are medications, radioactive iodine and thyroidectomy. The common side effect of radioactive iodine and thyroidectomy is hypothyroidism. The patient will need to take thyroid hormone supplement to restore normal hormone levels.
What are the symptoms of Hyperthyroidism?
Symptoms of hyperthyroidism vary from person to person. Usual signs include the following:
- Goiter
- Increased appetite, but weight loss
- Palpitation
- Hypertension
- Increased sensitivity to heat and perspiration
- Nervousness, anxiety or irritability, difficulty sleeping
- Hand tremors
- Fatigue, muscle weakness
- Changes in menstrual patterns (usually lighter flow, less frequent periods) in women
Other health problems may also cause these symptoms. Only a doctor can tell for sure. A person with any of these symptoms should tell the doctor so that the problems can be diagnosed and treated as early as possible.
Who is at highest risk?
- Graves’ disease
- Thyroid nodules
- Thyroiditis
- Too much iodine ingestion
- Over-medicating with synthetic thyroid hormone
Diagnosis
- Thyroid-Stimulating Hormone (TSH) test: This is a very sensitive and useful test and usually used as the first test to identify the disorder. The TSH test is based on the feedback between TSH and thyroid hormone. Patients with hyperthyroidism may show a lower reading than normal people.
- T3 and T4 test: This test may show the levels of T3 and T4 in your blood. In patients with hyperthyroidism, the levels of one or both of these hormones in your blood will be higher than normal.
- Thyroid-stimulating immunoglobulin (TSI) test: This test may help diagnose Graves' disease, which has this kind of antibody.
- Radioactive iodine uptake test: This test can detect the iodine uptake function of your thyroid gland and help diagnose the cause of hyperthyroidism. For example, low levels of iodine uptake might be a sign of thyroiditis, whereas high levels could indicate Graves’ disease.
- Thyroid scan: This test may also help diagnose the cause of hyperthyroidism by providing images of nodules and other possible thyroid irregularities.
Other diseases with similar symptoms:
- Autonomic nerve dysfunction
- Coronary artery disease
- Goiter
- Schizophrenia
- Thyroid cancer
When to seek urgent medical care?
Call your health care provider if symptoms of hyperthyroidism develop. If you experience either of the following symptoms, seeking urgent medical care as soon as possible:
- Palpitation
- Severe hypertension
Treatment options
Usual treatment measures of hyperthyroidism include medications, radioactive iodine, and surgery. Treatment options depend on the cause, age, physical condition and the severity of symptoms.
- Medications: Antithyroid medications, such as methimazole (Tapazole) and propylthiouracil (PTU), are used to block the production of thyroid hormone. Symptoms may begin to improve in 6 to 12 weeks and the whole treatment period may last for at least a year. Beta blockers, for example propranolol, may be used to relieve symptoms such as palpitation, nervousness,hypertension, sweating and shaking.
- Radioactive iodine: This kind of treatment may destroy the thyroid gland and stop the excess production of hormones. During this period, the patient takes radioactive iodine by mouth. A common side effect is permanent hypothyroidism, which needs thyroid supplements.
- Surgery: Thyroidectomy is another type of treatment option. The possible side effect after surgery is hypothyroidism. Patients need to take thyroid hormone supplements to restore normal hormone levels.
Contraindicated medications
Patients diagnosed with hyperthyroidism should avoid using the following medications:
- Levothyroxine
- Phentermine
If you have been diagnosed with hyperthyroidism, consult your physician before starting or stopping any of these medications.
Where to find medical care for Hyperthyroidism?
Directions to Hospitals Treating Hyperthyroidism
Prevention
- For hyperthyroidism caused by too much iodine ingestion, the method of prevention is decreasing iodine ingestion and a regular check of thyroid hormone levels in the blood.
- For hyperthyroidism caused by over-medicating with synthetic thyroid hormone, giving the appropriate dose to patients and a regular check of thyroid hormone levels in the blood may be important.
What to expect (Outlook/Prognosis)?
Many cases of hyperthyroidism are generally treatable. Prognosis depends on whether or not the patient has severe complications.
Possible Complications
Sources
- http://www.endocrine.niddk.nih.gov/pubs/Hyperthyroidism/
- http://www.nlm.nih.gov/medlineplus/ency/article/000356.htm
Causes
Major causes in humans are:
Other causes of hyperthyroxinemia (high blood levels of thyroid hormones) are not to be confused with true hyperthyroidism and include subacute and other forms of thyroiditis (inflammation) and struma ovarii (a teratoma). Thyrotoxicosis (symptoms caused by hyperthyroxinemia) can occur in both hyperthyroidism and thyroiditis. When it causes acutely increased metabolism, it is sometimes called "thyroid storm", a life-threatening event characterized by tachycardia, hypertension, and fever.
Excess thyroid hormone from pills can also cause hyperthyroidism. Amiodarone, a heart medication, can sometimes cause hyperthyroidism. Hamburger toxicosis is a condition that occurs sporadically and is associated with ground beef contaminated with thyroid hormone.
Postpartum thyroiditis occurs in about 7% of women during the year after they give birth. PPT typically has several phases, the first of which is hyperthyroidism. Many times, the hyperthyroidism corrects itself within weeks or months without any treatment necessary.
Life Threatening Causes
- Adenocarcinoma
- Choriocarcinoma
- Metastatic follicular thyroid cancer
- Pituitary tumor
- Struma ovarii
- Teratoma
- Testicular cancer
- Thyroid adenoma
- Thyroid carcinoma
- Thyroid nodule
- Thyroid tumor
- Thyrotropinoma
- Toxic adenoma
- Toxic thyroid adenoma
- Trophoblastic disease
- Tsh-producing pituitary adenoma
Common Causes
Causes by Organ System
Causes in Alphabetical Order
Calssification
Classification
Hyperthyroidism can be classified according to the results of iodine uptake test into:
High iodine uptake
- Grave’s disease
- Toxic multinodular goiter
- Toxic thyroid adenoma
High or normal uptake:
![Normal thyroid scan - Myohan at en.wikipedia [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons](/index.php/File:Thyroid_scan.jpg) |
- Iodine caused hyperthyroidism
- Hashitoxicosis
- Germ cell tumors (choriocarcinoma in males and testicular germ cell tumors)
- Pituitary TSH-producing adenoma
Low uptake
- Subacute thyroiditis
- Hyperthyroidism due to ectopic thyroid tissue
Pathophysiology
Thyroid hormones (T3 and T4) are regulating basal metabolic rate, influence oxygen consumption by tissues. They are crucial for normal development of the brain and growth of the body especially in prepubertal period.
Secretion of thyroid hormones follows upper control from the hypothalamus and the pituitary. Thyroid releasing hormone (TRH). TRH acts on thyrotropes releasing cells in the pituitary causing them to release thyroid stimulating hormone (TSH).
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TSH acts on thyroid gland by binding to specific membrane receptors and activating an intracellular pathway involving cAMP that ends in formation and secretion of thyroid hormones.
Iodine is essential for synthesis of thyroid hormones. The daily iodide need is about 100mcg / day. Iodide is uptaken through a special Na/I transporter found in the membrane of thyroid follicular cell. After uptaking iodide, it goes through a series of organic reactions ending in the formation of the two forms of thyroid hormones :T3 and T4. T3 and T4 remain stored in the thyroglobulin of the follicles and are released in response to further stimulation by TSH to the thyroid follicles.
While T3 is 3 to 5 times more potent than T4, it represents only one fourth of the total hormone secretion. T3 is thought to be the biologically active form of the of the two forms of the hormone. Most of the circulating T3 is due to peripheral conversion of T4 in the liver and peripheral tissues while only a small percentage is secreted directly from the thyroid gland itself.
T3 and T4 act on nuclear receptors (DNA binding proteins) and cause the regulate the transcription of many proteins to regulate the metabolic rate of the body.
The higher regulation of thyroxin secretion follows the negative feedback role, meaning that high levels of T3 and T4 will suppress TRH and TSH secretion and vice versa (Low levels of thyroxins will stimulate TRH and TSH secretion). This is useful in diagnosing the cause of hyperthyroidism (in secondary hyperthyroidism where the pituitary or the hypothalamus are the source of the disease. TSH will be high, while in primary hyperthyroidism where gland is the source of the excess hormones, TSH will be low).
In grave’s disease, the most common cause of hyperthyroidism. The disorder lies in the secretion of thyroid stimulating antibodies (TSI) that work on thyroid follicular cells causing excessive uncontrolled release of the thyroxins. TSI responsible for many other aspects of the disease such as ophthalmopathy and the skin manifestations. This is thought to be due to the epitopic similarity between antigens on the surface of these cells and the thyroid receptors.
The majority of circulating T3 and T4 are bound to plasma proteins and thus not active (T4 is mostly bound to thyroxine binding globulin and T3 is mostly bound to transthyretin). Conditons that impair the production of thyroid binding globulins (such as pregnancy, liver failure and certain drug administration) cause a change in the total serum thyroxins but the free T3 and T4 remain normal and patient remains euthyroid (this carries only laboratory significance).