Introduction
Background
In 1656, Thomas Wharton described the distinct nature of what he termed the thyroid gland, distinguishing it from the larynx, as this structure had been considered a laryngeal gland from the time of Andreas Vesalius in the 16th century. It was nearly 200 more years before the function of the thyroid was elucidated. The normal adult thyroid gland weighs 10-25 g and has 2 lobes connected by an isthmus. Nearly 50% of thyroid glands exhibit a pyramidal lobe arising from the center of the isthmus. Longitudinal dimensions of the lobes of the thyroid range up to 5 cm.
A goiter is an enlarged thyroid gland, and it may be diffuse or nodular. A goiter may extend into the retrosternal space, with or without substantial anterior enlargement. Because of the anatomic relationship of the thyroid gland to the trachea, larynx, superior and inferior laryngeal nerves, and esophagus, abnormal growth may cause a variety of compressive syndromes. Thyroid function may be normal (nontoxic goiter), overactive (toxic goiter), or underactive (hypothyroid goiter).
Pathophysiology
The thyroid gland is controlled by thyrotropin (TSH), secreted from the pituitary gland, which, in turn, is influenced by the thyrotropin-releasing hormone (TRH) from the hypothalamus. TSH permits growth, cellular differentiation, and thyroid hormone production and secretion by the thyroid gland. Thyrotropin acts on TSH receptors located on the thyroid gland. Serum thyroid hormones levothyroxine and triiodothyronine feed back to the pituitary, regulating TSH production. Interference with this TRH-TSH thyroid hormone axis causes changes in the function and structure of the thyroid gland. Stimulation of the TSH receptors of the thyroid by TSH, TSH-receptor antibodies, or TSH receptor agonists, such as chorionic gonadotropin, may result in a diffuse goiter. When a small group of thyroid cells, inflammatory cells, or malignant cells metastatic to the thyroid is involved, a thyroid nodule may develop.
A deficiency in thyroid hormone synthesis or intake leads to increased TSH production. Increased TSH causes increased cellularity and hyperplasia of the thyroid gland in an attempt to normalize thyroid hormone levels. If this process is sustained, a goiter is established. Causes of thyroid hormone deficiency include inborn errors of thyroid hormone synthesis, iodine deficiency, and goitrogens.
Goiter may result from a number of TSH receptor agonists. TSH receptor stimulators include TSH receptor antibodies, pituitary resistance to thyroid hormone, adenomas of the hypothalamus or pituitary gland, and tumors producing human chorionic gonadotropin.
Frequency
United States
Autopsy studies suggest a frequency of greater than 50% for thyroid nodules; with high-resolution ultrasound, the value approaches 40% of patients with nonthyroidal illness. In the Wickham study from the United Kingdom, 16% of the population had a goiter. In the Framingham study, ultrasonography revealed that 3% of men older than 60 years had thyroid nodules, while 36% of women aged 49-58 years had thyroid nodules. In the United States, most goiters are due to autoimmune thyroiditis (ie, Hashimoto disease).
International
Worldwide, the most common cause of goiter is iodine deficiency. It is estimated that goiters affect as many as 200 million of the 800 million people who have a diet deficient in iodine.
Mortality/Morbidity
Most goiters are benign, causing only cosmetic disfigurement. Morbidity or mortality may result from compression of surrounding structures, thyroid cancer, hyperthyroidism, or hypothyroidism.
Race
No racial predilection exists.
Sex
The female-to-male ratio is 4:1.
- In the Wickham study, 26% of women had a goiter, compared to 7% of men.
- Thyroid nodules are less frequent in men than in women, but when found, they are more likely to be malignant.
Age
The frequency of goiters decreases with advancing age. The decrease in frequency differs from the incidence of thyroid nodules, which increases with advancing age.
Clinical
History
A goiter may present in various ways, including the following:
- Incidentally, as a swelling in the neck discovered by the patient or on routine physical examination
- A finding on imaging studies performed for a related or unrelated medical evaluation
- Local compression causing dysphagia, dyspnea, stridor, plethora or hoarseness
- Pain due to hemorrhage, inflammation, necrosis, or malignant transformation
- Signs and symptoms of hyperthyroidism or hypothyroidism
- Thyroid cancer with or without metastases
Physical
The general examination for hyperthyroidism, hypothyroidism, and autoimmune stigmata is followed by systematic examination of the goiter.
- A retrosternal goiter may not be evident on physical examination.
- Examination of the goiter is best performed with the patient upright, sitting or standing. Inspection from the side may better outline the thyroid profile (see Image 1). Asking the patient to take a sip of water facilitates inspection. The thyroid should move upon swallowing.
- Palpation of the goiter is performed either facing the patient or from behind the patient, with the neck relaxed and not hyperextended. Palpation of the goiter rules out a pseudogoiter, which is a prominent thyroid seen in individuals who are thin. Each lobe is palpated for size, consistency, nodules, and tenderness. Cervical lymph nodes are then palpated. The oropharynx is visualized for the presence of lingular thyroid tissue.
- The size of each lobe is measured in 2 dimensions using a tape measure. Some examiners make tracings on a sheet of paper, which is placed in the patient's chart. Suitable landmarks are used and documented to ensure consistent measurement of the thyroid gland.
- The pyramidal lobe often is enlarged in Graves disease.
- A firm rubbery thyroid gland suggests Hashimoto thyroiditis, and a hard thyroid gland suggests malignancy or Reidel struma.
- Multiple nodules may suggest a multinodular goiter or Hashimoto thyroiditis. A solitary hard nodule suggests malignancy, whereas a solitary firm nodule may be a thyroid cyst.
- Diffuse thyroid tenderness suggests subacute thyroiditis, and local thyroid tenderness suggests intranodal hemorrhage or necrosis.
- Cervical lymph glands are palpated for signs of metastatic thyroid cancer.
- Auscultation of a soft bruit over the inferior thyroidal artery may be appreciated in a toxic goiter. Palpation of a toxic goiter may reveal a thrill in the profoundly hyperthyroid patient.
- Goiters are described in a variety of ways, including the following:
- Toxic goiter: A goiter that is associated with hyperthyroidism is described as a toxic goiter. Examples of toxic goiters include diffuse toxic goiter (Graves disease), toxic multinodular goiter, and toxic adenoma (Plummer disease).
- Nontoxic goiter: A goiter without hyperthyroidism or hypothyroidism is described as a nontoxic goiter. It may be diffuse or multinodular, but a diffuse goiter often evolves into a nodular goiter. Examination of the thyroid may not reveal small or posterior nodules. Examples of nontoxic goiters include chronic lymphocytic thyroiditis (Hashimoto disease), goiter identified in early Graves disease, endemic goiter, sporadic goiter, congenital goiter, and physiologic goiter that occurs during puberty.
- Autonomously functioning nodules may present with inability to palpate the contralateral lobe. Unilobar agenesis may also present like a single thyroid nodule with hyperplasia of the remaining lobe.
- The Pemberton maneuver raises a goiter into the thoracic inlet when the patient elevates the arms. This may cause shortness of breath, stridor, or distention of neck veins.
Causes
The different etiologic mechanisms that can cause a goiter include the following:
- Iodine deficiency
- Autoimmune thyroiditis - Hashimoto or postpartum thyroiditis
- Excess iodine (Wolff-Chaikoff effect) or lithium ingestion, which decrease release of thyroid hormone
- Goitrogens
- Stimulation of TSH receptors by TSH from pituitary tumors, pituitary thyroid hormone resistance, gonadotropins, and/or thyroid-stimulating immunoglobulins
- Inborn errors of metabolism causing defects in biosynthesis of thyroid hormones
- Exposure to radiation
- Deposition diseases
- Thyroid hormone resistance
- Subacute thyroiditis (de Quervain thyroiditis)
- Silent thyroiditis
- Riedel thyroiditis
- Infectious agents
- Acute suppurative - Bacterial
- Chronic - Mycobacteria, fungal, and parasitic
- Granulomatous disease
- Thyroid malignancy
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Schumm-Draeger PM. [Every third German has a sick thyroid gland. Nodules and goiter are a challenge that needs to be met]. MMW Fortschr Med. Feb 5 2004;146(6):20. [Medline].
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Further Reading
Keywords
thyroid gland goiter, nontoxic goiter, toxic goiter, multinodular goiter, endemic goiter, Hashimoto disease, iodine, enlarged thyroid gland, inborn errors of thyroid hormone synthesis, iodine deficiency, goitrogens, TSH receptor antibodies, pituitary resistance to thyroid hormone, adenomas of hypothalamus, adenomas of pituitary gland, tumors producing human chorionic gonadotropin, autoimmune thyroiditis, Hashimoto disease, thyroid cancer, hyperthyroidism, hypothyroidism, thyroid nodules, swelling in the neck,
