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Hypothyroidism and Goiters
by Anna M. Salanti
Goiters are caused by an increase in the size of the thyroid gland. The thyroid gland produces thyroxin that regulates all aspects of your metabolism. Goiters can occur whether the thyroid gland produces too little, too much, or normal amounts of thyroxin. The pituitary gland secretes thyroid stimulating hormone (TSH) as a response to the circulating amounts of thyroxin in the blood. TSH will also stimulate the thyroid to secrete more thyroxin and can cause the thyroid gland to grow. Cysts and tumors can also enlarge a part of the thyroid gland.
Goiters are either diffuse, involving the entire gland without evidence of nodularity, or they can contain nodules. Diffuse goiters usually become nodular. Goiters can be either toxic or nontoxic. A toxic goiter will produce signs of extreme hyperthyroidism. Diffuse nontoxic and multi-nodular goiters are the outcome of compensatory hypertrophy and hyperplasia of follicular epithelium from some disorder of thyroid hormone output.
The size of the goiter is usually proportional to the degree and duration of the thyroid imbalance. Multinodular goiters are usually the largest in size and are associated with thryotoxicosis. As goiters grow, they can become large enough to compress the esophagus, trachea, and the superior vena cava. When the trachea and esophagus are compressed, the individual may experience difficulty swallowing, inspiratory stridor, awakening at night with the sensation of being unable to breathe, and sensation of choking. If the vena cava is compressed, the following symptoms can occur: distended neck and upper extremity vein distention, eyelid and conjunctiva swelling, and syncope with coughing.
The most common cause of a goiter in the early part of the 20th century was a lack of iodine in the diet in areas where the soil was deficient in iodine. Iodine is essential in order for the thyroid to make and release two essential iodine-containing hormones—thyroxin and triodotyronine (T3). After the addition of iodine to salt in the United States in the 1920s, goiter became a rare occurrence. In some parts of underdeveloped countries, goiter is a much more common occurrence.
Iodine occurs naturally in certain foods such as seafood, dairy products, and water. Some foods contain substances that interfere with thyroid hormone synthesis. Some varieties of turnips and cabbage have this effect, but clinically their significance is minimal. If the dietary iodine intake is suddenly increased in the case of an iodine deficient goiter, the thyroid may suddenly make large amounts of thyroxin and cause a thyroid storm.
A normally functioning thyroid gland will produce thyroxin and T3. These hormones circulate in your bloodstream and regulate your metabolism. The pituitary gland and hypothalamus control the production and the rate of thyroxin and T3 release. The hypothalamus stimulates the pituitary to produce thyroid stimulating hormone (TSH). Depending on the amounts of thyroxin and T3 in the blood, the pituitary gland will release a specific amount of TSH. The thyroid gland will then regulate the production of thyroxin and T3 based on the amount of TSH it receives from the pituitary gland.
Goiters occur in hypothyroid, euthyroid, and hyperthyroid conditions. In a hyperthyroid goiter, the amount of TSH is excessive and will cause the thyroid gland to produce too much thyroxin and enlarge. Grave's disease is a most common form of this disorder.
If dietary iodine is slightly deficient, too little thyroxin will be secreted, stimulating the pituitary to produce more TSH. The end result is a thyroid gland that enlarges sufficiently to produce enough thyroxin. If the dietary iodine intake is severely reduced, the thyroid gland will enlarge but will be unable to produce the needed amounts of thyroxin. The thyroid gland will continue to grow as a result of TSH stimulation but will not be able to produce enough thyroxin.
There are many other causes of goiter other than iodine deficiency. Listed below are some of the more common causes of goiter:
- Graves's disease: an autoimmune disorder that is the most common cause of hyperthyroidism. The antibodies produced by the individual's immune system stimulate the thyroid to produce too much thyroxin. Antibodies are normally protective, but in Grave's disease the antibodies attack the thyroid gland and at times the tissues behind the eyes and the skin of lower legs.
- Hashimoto's disease: also known as chronic lymphocytic thyroiditis. This is a very common cause of hypothyroidism. Like Grave's disease, it is an autoimmune disease which causes inflammation of the thyroid gland. The inflammation impairs the thyroid's ability to produce hormones causing the pituitary to compensate by stimulating the thyroid gland to produce more hormones. The end result of this process is the development of a goiter.
- Multinodular goiter: the development of multiple nodules in both sides of the thyroid. This condition can occur with normal, low, or excessive thyroid hormone production.
- Solitary thyroid nodules: a single nodule that occurs in any area of the thyroid gland. These nodules are typically benign.
- Thyroid cancer: this condition occurs less frequently than benign nodules. An enlargement on one side of the thyroid is the typical appearance of thyroid cancer.
- Pregnancy: during pregnancy, human chorionic gondadotropin (HCG) can cause uniform enlargement of the thyroid gland.
- Inflammation: this condition is called thyroiditis and there are various types.
References:
http://www.merck.com/mrkshared/mmanual/section2/chapter8/8b.jsp (Euthyroid goiter)
http://www.merck.com/mrkshared/mmanual/section2/chapter8/8d.jsp (Grave's disease or non-toxic goiter)
http://www.merck.com/mrkshared/CVMHighLight?file=/mrkshared/mmanual/section2/
chapter8/8f.jsp%3Fregion%3Dmerckcom&word=hypothyroid&word=goiter&domain=
www.merck.com#hl_anchor (hypothyroid goiter)
http://www.healthatoz.com/healthatoz/Atoz/ency/goiter.jsp (hypo & hyper)
http://www.endocrineweb.com/hypo1.html (hypo)
http://www.cnn.com/HEALTH/library/DS/00217.html (hypo & hyper)
Copstead, L. C. and Banasik, J. L. (2005). Pathophysiology. St. Louis, MO. Elsevier Saunders.
Porth, C.M. (2005). Pathophysiology Concepts of Altered Health States. Philadelphia, PA. Lippincott Williams & Wilkins.
This article has been reprinted with permission from Anna M. Salanti.
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