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A goiter is an enlarged thyroid gland, one of several physical changes the thyroid can undergo, usually in association with overstimulation along the hypothalamic–pituitary–thyroid (HPT) axis. The constant stimulation of the thyroid to produce more hormones causes proliferation of the cells where thyroid hormones are synthesized, to increase T4 production. The proliferation of these cells and the development of a goiter may also be traced to iodine deficiency.
Physical signs and symptoms of goiter may include an obvious bulge in the neck, choking sensation while consuming food, occasional pain in the neck, hoarseness, discomfort with clothing or jewelry worn close to the neck, and a vibrating sensation.
The development of a lump in the thyroid, called a thyroid nodule, occurs as a result of abnormal proliferation of thyroid cells. Nodules are usually not cancerous, but because they can sometimes signify the development of a thyroid malignancy, they should always be carefully evaluated for potential cancerous cell growth.
Most often, thyroid nodules do not present with specific symptoms apart from a slightly noticeable lump. Nor are the underlying causes of noncancerous thyroid lumps well-defined. While patients with hypothyroidism may develop a thyroid nodule, this is not usually the case. In some cases lack of dietary iodine intake may be a contributing cause. Nodules can also develop autonomously as a result of genetic predisposition.
Thyroid nodules can lead to either hyperthyroidism or hypothyroidism, depending on whether the thyroid cells within the lump are "cold" or "hot," as detected on thyroid scanning. The cells in "hot" nodules release hormones in an uncontrolled way, no longer regulated properly by the normal signals. This leads to hyperthyroidism. Conversely, "cold" nodules produce little to no hormones, thus contributing to hypothyroidism. The presence of "warm" nodules on scanning implies normal thyroid function.
Malignant thyroid tissue or nodules in the thyroid complex can be categorized into four main types of thyroid cancer: follicular, papillary, medullary, and anaplastic. Genetic associations and toxic exposures rank among potential causes of thyroid cancer, but originating causes of thyroid cancer diseases are multifactorial and not well understood.
Some of the primary symptoms of thyroid cancer include persistent pain in the neck, swollen lymph nodes, problems with swallowing, formation of a lump near the Adam's apple, and hoarseness.
Thyroid cancer is often detected following the development of thyroid nodules on the gland. Statistically, thyroid nodules are quite common, found in an estimated 40–50% of the asymptomatic population by one report. The vast majority of these lumps are benign and cause no symptoms at all. Still, a medical work-up is recommended to ascertain their nature. A physician may perform ultrasound or biopsy to more closely evaluate a nodule and obtain information.
Four different types of thyroid cancers can potentially cause thyroid hormone imbalance and thyroid gland enlargement. The most common is papillary thyroid cancer, which accounts for approximately 60% of thyroid cancer cases. Papillary tumors are cystic masses that form from otherwise normal thyroid hormone-producing tissue and tend to stay fairly localized. Follicular thyroid cancers, however, which account for 12% of thyroid cancer cases, are more invasive and more likely to spread to other parts of the body.The above two types of well-differentiated thyroid cancer are usually curable. Medullary thyroid cancers occur in the parafollicular cells of the thyroid, which produce the hormone calcitonin. Anaplastic thyroid cancers are the rarest form but most invasive of thyroid cancer, and have the poorest prognosis for patients. Advances in cancer medicine as well as integrative treatment protocols are helping to minimize associated health risks to patients with thyroid cancer.
Thyroiditis is a general term that refers to inflammation of the thyroid gland tissues. The thyroid gland may become swollen, tender, and painful to touch, and the person may develop a fever. Sometimes thyroiditis is also accompanied by symptoms of hyperthyroidism or hypothyroidism.
The inflammation of thyroiditis arises as a consequence of abnormal activity on the part of the body's immune system. Immune cells may create several types of anti-thyroid antibodies (autoantibodies) that attack the thyroid gland, leading to damage and eventual destruction of the thyroid cells.
There are several types of thyroiditis. Specific symptoms depend on the type and stage of thyroiditis. The underlying causes of thyroiditis also vary, depending on the type. Of the five main forms of thyroiditis, Hashimoto's Disease, (also known as Hashimoto's Thyroiditis) is the most common. Hashimoto's, the disease, is often cited as the most common cause of hypothyroidism, the condition. In the United States, genetics are strongly implicated as a cause of Hashimoto's disease.
Patients with Hashimoto's frequently experience hypothyroidism, sometimes alternating with bouts of hyperthyroidism. Symptoms may include fatigue, muscle weakness or cramps, slow or fast heart beat, sensitivity to heat and/or to cold, weight gain, high cholesterol, hypoglycemia, constipation, migraine headaches, hair loss, memory problems, anxiety, depression, mania, or panic attacks. Because of the extensive range of effects and symptoms of Hashimoto's, including those involving mood and affect, people with Hashimoto's thyroiditis are often misdiagnosed with depression, PMS, bipolar disorder, or anxiety. Difficulties with diagnosis can be avoided or resolved with appropriate testing to include TSH and anti-thyroid antibodies.
Postpartum thyroiditis is thought to stem from changes in the immune system that occur to accommodate pregnancy.Prevalence of this form of thyroiditis varies by region and survey design, but about 7% of all pregnancies result in this condition. In the New York metropolitan region, the general prevalence of postpartum thyroiditis is a little higher, at 8.8%, and in women with Type I diabetes in this area, prevalence jumps to 25%.
Interestingly, postpartum thyroiditis represents an exacerbation of an underlying autoimmune thyroiditis that was clinically "silent" prior to pregnancy. During pregnancy the body undergoes partial immunosuppression to allow the fetus to be carried successfully to term. Following birth, the mother's immune system rebounds, "aggravating" the previously silent condition.
Postpartum thyroiditis may cause transient hyperthyroidism or transient hypothyroidism, or both, as the woman's body rebalances itself. Most women return to normal thyroid output during the year following the pregnancy. However, some may retain the imbalance and require lifelong treatment for a persistent thyroid condition. Recurrence following ensuing pregnancies is very common.
Postpartum cases of Graves' disease are about 20 times less common than postpartum thyroiditis; however, Graves' disease does occur more frequently postpartum than at other times. In addition, because 1 in 4 women with postpartum thyroiditis test positive for TSH receptor antibody, an overlapping sign between the two, diagnosis is not always straightforward. An endocrinologist can correctly make the differential diagnosis through careful physical exam, sometimes in conjunction with further testing using radionuclide uptake.
A bacterial or viral infection that spreads to the thyroid and causes inflammation can less frequently be the originating cause of thyroiditis, and may lead to increased release of thyroid hormones, or progress with other dysfunction such as fatigue or cognitive impairment. In genetically predisposed individuals, DeQuervain's thyroiditis, also known as subacute thyroiditis (SAT), is believed to arise following upper respiratory infection with influenza virus, adenovirus, Coxsackie virus, Epstein–Barr or cytomegaloviruses, with certain genetic variants playing an important role.
Hyperthyroidism is the medical term for an overactive thyroid gland, when the thyroid releases an excess of thyroid hormones.
The most common cause of hyperthyroidism is an autoimmune disorder called Graves' disease. In patients with this condition, the immune system develops autoantibodies to the thyrotropin receptors on the thyroid gland. Under normal (euthyroid, meaning "well thyroid") conditions, thyroid-stimulating hormone (TSH) produced by the pituitary gland binds to these receptors, to stimulate the thyroid into producing thyroid hormones. TSH is released in a controlled fashion from the pituitary gland, resulting in controlled stimulation of thyroid hormone production. In patients with Graves' disease, however, the autoantibodies produced by this abnormal immune system response bind with and continuously stimulate the thyrotropin receptors, resulting in overproduction of thyroid hormones.
The originating cause of this abnormal immune response in Graves' disease is unknown, although there appears to be a strong hereditary component. Some patients develop hyperthyroidism following a severely stressful life event; but while there may be an emotional component for some patients, others report no triggering event.
Hypothyroidism is the medical term for an underactive thyroid gland. Low thyroid function leads to insufficient thyroid hormone production, which frequently causes weight gain through slowed metabolism and water retention. Low thyroid hormone levels may also result in thinning hair, brittle nails, pale skin, poor muscle tone, and low heart rate. Energy levels may be quite low, frequently leading to fatigue even in the absence of exertion. Muscle cramping, painful joints, and sensitivity to cold can also result from hypothyroidism. The thyroid hormone T3 also influences serotonin levels, a neurotransmitter that helps define mood, and insufficient T3 can thus be associated with low mood or depression.
Another potential problem caused by hypothyroidism is the development of a goiter, a swelling of the thyroid gland that occurs due to excessive stimulation of thyroid cells by thyroid-stimulating hormone (TSH). A normally functioning thyroid gland would respond to the TSH by producing thyroid hormones which would, in turn, through a normal negative feedback loop, turn off the release of TSH. In the case of hypothyroidism, however, because physiologic thyroid hormone levels are never restored, TSH stimulation does not cease. As a result, the cells in the thyroid gland divide unchecked, causing the thyroid lobes to increase in size and eventually, to bulge from the neck. It can also cause the eyes to begin to protrude.
About 3 out of 100 people have hypothyroidism. Historically, insufficient iodine intake was the primary cause of hypothyroidism, and although the US population is generally considered iodine-sufficient, iodine deficiency is again on the upswing, of particular concern among women of childbearing age and the elderly. An estimated 1 in 7 women in the US may be deficient. Deficiency is due to factors that include topsoil depletion and low dietary intake, and environmental and dietary exposure to a range of chemicals in the halide family containing fluoride, chlorine, and bromine have also been associated with iodine displacement in the body. Iodine is an integral component of thyroid hormones T3 and T4, and these major thyroid hormones cannot be synthesized in its absence.
The most common type of hypothyroidism in individuals with adequate iodine levels is Hashimoto's thyroiditis, an autoimmune disorder in which the body mounts an immune response to the cells of the thyroid gland. As its cells are destroyed, the thyroid becomes progressively less functional, causing T3 and T4 levels to drop far below normal. A few specific genes involved in the regulation and specificity of the immune response have been implicated in increasing the risk of Hashimoto's thyroiditis.
Types and Causes of Thyroid Problems—Citations and Further Reading