Ruchi Mathur, MD, FRCP(C)
Ruchi Mathur, MD, FRCP(C)
Ruchi Mathur, MD, FRCP(C) is an Attending Physician with the Division of Endocrinology, Diabetes and Metabolism and Associate Director of Clinical Research, Recruitment and Phenotyping with the Center for Androgen Related Disorders, Department of Obstetrics and Gynecology at Cedars-Sinai Medical Center.
William C. Shiel Jr., MD, FACP, FACR
William C. Shiel Jr., MD, FACP, FACR
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
In this Article
Thyroid hormone regulation--the chain of command
The thyroid itself is regulated by another gland located in the brain, called the pituitary. In turn, the pituitary is regulated in part by thyroid hormone that is circulating in the blood (a "feedback" effect of thyroid hormone on the pituitary gland) and in part by another gland called the hypothalamus, also a part of the brain.
The hypothalamus releases a hormone called thyrotropin releasing hormone (TRH), which sends a signal to the pituitary to release thyroid stimulating hormone (TSH). In turn, TSH sends a signal to the thyroid to release thyroid hormones. If overactivity of any of these three glands occurs, an excessive amount of thyroid hormones can be produced, thereby resulting in hyperthyroidism.
Hypothalamus - TRH↓
Thyroid- T4 and T3
The rate of thyroid hormone production is controlled by the pituitary gland. If there is an insufficient amount of thyroid hormone circulating in the body to allow for normal functioning, the release of TSH is increased by the pituitary in an attempt to stimulate the thyroid to produce more thyroid hormone. In contrast, when there is an excessive amount of circulating thyroid hormone, the release of TSH is reduced as the pituitary attempts to decrease the production of thyroid hormone.
What causes hyperthyroidism?
Some common causes of hyperthyroidism include:
Graves' disease, which is caused by a generalized overactivity of the thyroid gland, is the most common cause of hyperthyroidism. In this condition, the thyroid gland usually is renegade, which means it has lost the ability to respond to the normal control by the pituitary gland via TSH. Graves' disease is hereditary and is up to five times more common among women than men. Graves' disease is thought to be an autoimmune disease, and antibodies that are characteristic of the illness may be found in the blood. These antibodies include thyroid stimulating immunoglobulin (TSI antibodies), thyroid peroxidase antibodies (TPO), and TSH receptor antibodies. The triggers for Grave's disease include:
Graves' disease can be diagnosed by a standard, nuclear medicine thyroid scan which shows diffusely increased uptake of a radioactively-labeled iodine. In addition, a blood test may reveal elevated TSI levels.
Grave's disease may be associated with eye disease (Graves' ophthalmopathy) and skin lesions (dermopathy). Ophthalmopathy can occur before, after, or at the same time as the hyperthyroidism. Early on, it may cause sensitivity to light and a feeling of "sand in the eyes." The eyes may protrude and double vision can occur. The degree of ophthalmopathy is worsened in those who smoke. The course of the eye disease is often independent of the thyroid disease, and steroid therapy may be necessary to control the inflammation that causes the ophthalmopathy. In addition, surgical intervention may be required. The skin condition (dermopathy) is rare and causes a painless, red , lumpy skin rash that appears on the front of the legs.
Functioning Adenoma and Toxic Multinodular Goiter
The thyroid gland (like many other areas of the body) becomes lumpier as we get older. In the majority of cases, these lumps do not produce thyroid hormones and require no treatment. Occasionally, a nodule may become "autonomous," which means that it does not respond to pituitary regulation via TSH and produces thyroid hormones independently. This becomes more likely if the nodule is larger that 3 cm. When there is a single nodule that is independently producing thyroid hormones, it is called a functioning nodule. If there is more than one functioning nodule, the term toxic, multinodular goiter is used. Functioning nodules may be readily detected with a thyroid scan.
Excessive intake of thyroid hormones
Taking too much thyroid hormone medication is actually quite common. Excessive doses of thyroid hormones frequently go undetected due to the lack of follow-up of patients taking their thyroid medicine. Other persons may be abusing the drug in an attempt to achieve other goals such as weight loss. These patients can be identified by having a low uptake of radioactively-labelled iodine (radioiodine) on a thyroid scan.
Abnormal secretion of TSH
A tumor in the pituitary gland may produce an abnormally high secretion of TSH (the thyroid stimulating hormone). This leads to excessive signaling to the thyroid gland to produce thyroid hormones. This condition is very rare and can be associated with other abnormalities of the pituitary gland. To identify this disorder, an endocrinologist performs elaborate tests to assess the release of TSH.
Thyroiditis (inflammation of the thyroid)
Inflammation of the thyroid gland may occur after a viral illness (subacute thyroiditis). This condition is association with a fever and a sore throat that is often painful on swallowing. The thyroid gland is also tender to touch. There may be generalized neck aches and pains. Inflammation of the gland with an accumulation of white blood cells known as lymphocytes (lymphocytic thyroiditis) may also occur. In both of these conditions, the inflammation leaves the thyroid gland "leaky," so that the amount of thyroid hormone entering the blood is increased. Lymphocytic thyroiditis is most common after a pregnancy and can actually occur in up to 8% of women after delivery. In these cases, the hyperthyroid phase can last from 4 to 12 weeks and is often followed by a hypothyroid (low thyroid output) phase that can last for up to 6 months. The majority of affected women return to a state of normal thyroid function. Thyroiditis can be diagnosed by a thyroid scan.
Excessive iodine intake
The thyroid gland uses iodine to make thyroid hormones. An excess of iodine may cause hyperthyroidism. Iodine-induced hyperthyroidism is usually seen in patients who already have an underlying abnormal thyroid gland. Certain medications, such as amiodarone (Cordarone), which is used in the treatment of heart problems, contain a large amount of iodine and may be associated with thyroid function abnormalities.
Medically Reviewed by a Doctor on 5/8/2014