Hyperthyroidism is a state in which the body is producing too much thyroid hormone. The main hyperthyroid conditions are:

- Graves' disease

- Toxic thyroid nodule

- Thyroid storm

- Toxic nodular struma (Plummer's disease)

- Hashitoxicosis: "transient" hyperthyroidism that can occur in Hashimoto's thyroiditis

Certain medications can have the unintended side effect of affecting thyroid function. While some medications can lead to significant hypothyroidism or hyperthyroidism and those at risk will need to be carefully monitored, some medications may affect thyroid hormone lab tests without causing any symptoms or clinical changes, and may not require treatment. The following medications have been linked to various forms of thyroid disease:

- Amiodarone (more commonly can lead to hypothyroidism, but can be associated with some types of hyperthyroidism)

- Lithium salts (hypothyroidism)

- Some types of interferon and IL-2 (thyroiditis)

- Glucocorticoids, dopamine agonists, and somatostatin analogs (block TSH, which can lead to hypothyroidism)

Solitary thyroid nodules are more common in females yet more worrisome in males. Other associations with neoplastic nodules are family history of thyroid cancer and prior radiation to the head and neck.

Most common cause of solitary thyroid nodule is benign colloid nodules and second most common cause is follicular adenoma.

Radiation exposure to the head and neck may be for historic indications such as tonsillar and adenoid hypertrophy, "enlarged thymus", acne vulgaris, or current indications such as Hodgkin's lymphoma. Children living near the Chernobyl nuclear power plant during the catastrophe of 1986 have experienced a 60-fold increase in the incidence of thyroid cancer. Thyroid cancer arising in the background of radiation is often multifocal with a high incidence of lymph node metastasis and has a poor prognosis.

85% of nodules are cold nodules, and 5–8% of cold and warm nodules are malignant.

5% of nodules are hot. Malignancy is virtually non-existent in hot nodules.

Thyroid cancers are thought to be related to a number of environmental and genetic predisposing factors, but significant uncertainty remains regarding their causes.

Environmental exposure to ionizing radiation from both natural background sources and artificial sources is suspected to play a significant role, and there are significant increased rates of thyroid cancer in those exposed to mantlefield radiation for lymphoma, and those exposed to iodine-131 following the Chernobyl, Fukushima, Kyshtym, and Windscale nuclear disasters. Thyroiditis and other thyroid diseases also predispose to thyroid cancer.

Genetic causes include multiple endocrine neoplasia type 2 which markedly increases rates, particularly of the rarer medullary form of the disease.

Sequence of events:

1. Iodine deficiency leading to decreased T4 production.

2. Induction of thyroid cell hyperplasia due to low levels of T4. This accounts for the multinodular goitre appearance.

3. Increased replication predisposes to a risk of mutation in the TSH receptor.

4. If the mutated TSH receptor is constitutively active, it would then become 'toxic' and produces excess T3/T4 leading to hyperthyroidism.

Thyroid cancer, in 2010, resulted in 36,000 deaths globally up from 24,000 in 1990. Obesity may be associated with a higher incidence of thyroid cancer, but this relationship remains the subject of much debate.

Thyroid cancer accounts for less than 1% of cancer cases and deaths in the UK. Around 2,700 people were diagnosed with thyroid cancer in the UK in 2011, and around 370 people died from the disease in 2012.

Women being treated for Hashimoto's disease can become pregnant. It is recommended that thyroid function be well-controlled before getting pregnant.

Untreated or poorly treated underactive thyroid can lead to problems for the mother, such as:

- Preeclampsia

- Anemia

- Miscarriage

- Placental abruption

- High cholesterol

- Postpartum bleeding

It also can cause serious problems for the baby, such as:

- Preterm birth

- Low birth weight

- Stillbirth

- Birth defects

- Thyroid problems

A cold nodule is a thyroid nodule that does not produce thyroid hormone. On a radioactive iodine uptake test a cold nodule takes up less radioactive material than the surrounding thyroid tissue. A cold nodule may be malignant or benign. On scintigraphy cold nodules do not show but are easily shown on ultrasound. Figure 1 illustrates the basic anatomy of the thyroid gland. The case shown in Figure 4 shows a cold nodule quite emphasized representation of the thyroid. The investigation was carried out due to a goiter rating of 3. Striking was the discrepancy between the magnification sonographically depicted the thyroid lobe and the findings in the scintigraphy; the lower part of the right lobe and the lateral part of the left missing in the bone scan, although demonstrably thyroid tissue is present there sonographically. This imperfective representation for thyroid tissue is the characteristic of "cold node".

Depending on source, the overall 5-year survival rate for medullary thyroid cancer is 80%, 83% or 86%, and the 10-year survival rate is 75%.

By overall cancer staging into stages I to IV, the 5-year survival rate is 100% at stage I, 98% at stage II, 81% at stage III and 28% at stage IV. The prognosis of MTC is poorer than that of follicular and papillary thyroid cancer when it has metastasized (spread) beyond the thyroid gland.

The prognostic value of measuring calcitonin and carcinoembryonic antigen (CEA) concentrations in the blood was studied in 65 MTC patients who had abnormal calcitonin levels after surgery (total thyroidectomy and lymph node dissection). The prognosis correlated with the rate at which the postoperative calcitonin concentration doubles, termed the calcitonin doubling time (CDT), rather than the pre- or postoperative absolute calcitonin level:

- CDT less than 6 months: 3 patients out of 12 (25%) survived 5 years. 1 patient out of 12 (8%) survived 10 years. All died within 6 months to 13.3 years.

- CDT between 6 months and 2 years: 11 patients out of 12 (92%) survived 5 years. 3 patients out of 8 (37%) survived 10 years. 4 patients out of 12 (25%) survived to the end of the study.

- CDT more than 2 years: 41 patients out of 41 (100%) were alive at the end of the study. These included 1 patient whose calcitonin was stable, and 11 patients who had decreasing calcitonin levels.

The calcitonin doubling time was a better predictor of MTC survival than CEA but following both tests is recommended.

Pregnant women who are positive for Hashimoto's thyroiditis may have decreased thyroid function or the gland may fail entirely. If a woman is TPOAb-positive, clinicians can inform her of the risks for themselves and their infants if they go untreated. "Thyroid peroxidase antibodies (TPOAb) are detected in 10% of pregnant women," which presents risks to those pregnancies. Women who have low thyroid function that has not been stabilized are at greater risk of having an infant with: low birth weight, neonatal respiratory distress, hydrocephalus, hypospadias, miscarriage, and preterm delivery. The embryo transplantion rate and successful pregnancy outcomes are improved when Hashimoto's is treated. Recommendations are to only treat pregnant women who are TPOAb-positive throughout the entirety of their pregnancies and to screen all pregnant women for thyroid levels. Close cooperation between the endocrinologist and obstetrician benefits the woman and the infant. The Endocrine Society recommends screening in pregnant women who are considered high-risk for thyroid autoimmune disease.

Thyroid peroxides antibodies testing is recommended for women who have ever been pregnant regardless of pregnancy outcome. "...[P]revious pregnancy plays a major role in development of autoimmune overt hypothyroidism in premenopausal women, and the number of previous pregnancies should be taken into account when evaluating the risk of hypothyroidism in a young women ["sic"]."

Normal hormone changes during pregnancy cause thyroid hormone levels to increase. The thyroid may enlarge slightly in healthy women during pregnancy, but not enough to be felt. These changes do not affect the pregnancy or unborn baby. Yet, untreated thyroid problems can threaten pregnancy and the growing baby. Symptoms of normal pregnancy, like fatigue, can make it easy to overlook thyroid problems in pregnancy.

Thyroid hormone is vital during pregnancy. The unborn baby's brain and nervous system need thyroid hormone to develop. During the first trimester, the baby depends on the mother's supply of thyroid hormone. At 10 to 12 weeks of pregnancy, the baby's thyroid begins to work on its own. But the baby still depends on the mother for iodine, which the thyroid uses to make thyroid hormone. Pregnant women need about 250 micrograms (mcg) of iodine a day. Some women might not get all the iodine they need through the foods they eat or prenatal vitamins. Using iodized salt — salt that has had iodine added to it over plain table salt is recommended. Prenatal vitamins that contain iodine are also recommended.

Some women develop thyroid problems in the first year after giving birth. This is called postpartum thyroiditis. It often begins with symptoms of an overactive thyroid, which last 2 to 4 months. Mild symptoms might be overlooked. Affected women then develop symptoms of an underactive thyroid, which can last up to a year. An underactive thyroid needs to be treated. In most cases, thyroid function returns to normal as the thyroid heals.

Toxic nodular goiter (TNG) (or toxic multinodular goiter, or Plummer's disease) is a condition that can occur when a hyper-functioning nodule develops within a longstanding goiter. This results in hyperthyroidism, without the eye bulging effects seen in Grave's disease. These toxic nodular goiters are most common in women over the age of 60.

It was named by Henry Stanley Plummer.

Toxic nodular goiter is the presence of thyrotoxicosis and thyroid nodules. It is prevalent in people older than 40 years old who have an iodine deficiency. There is a much higher incidence of TNG in European countries in comparison to the United States. This condition is not common in the United States and Canada due to the iodine addition in table salt. Americans consume much higher dosages of iodine compared to the 25–100 ug/day that Europeans consume.

TNG is caused by a toxic multinodular goiter. Autonomous thyroid nodules become hyper-functional from mutations in the follicular cell. The mutation activates cAMP (cyclic adenosine monophosphate), causing an increase in the cells' function and growth. This is different from the thyroid condition called Grave’s disease, as Grave’s disease causes a hyper-function from external factors such as immunoglobulin that activate the TSH receptors. Hyper-function of TSH, thyroid stimulating hormone, activates the thyroid, which in excess can cause a condition known as goiter. The nodules that form could be driven by a loss of inhibition or gain of function mutations; however, this is purely speculation as the cause is still unknown. These nodules are assumed to be irreversible and when functional can lead to thyrotoxicosis (another name for hyperthyroidism).

Thyrotoxicosis has been documented to have some cases of spontaneous remission without treatment as seen in the study done by Siegel and Lee. It is possible that the remission of thyrotoxicosis is a result of spontaneous hemorrhage and cystic degeneration. This situation means that bleeding would occur in the thyroid, which could cause the nodules to break down, reversing the symptoms. These results of spontaneous remission were contrary to the study’s previous results showing that the nodules were irreversible. Patients presenting symptoms of toxic nodular goiter can also be treated using the same procedures as hyperthyroidism.

Hyperthyroidism is very rare in dogs, occurring in less than 1% of dogs. Hyperthyroidism may be caused by a thyroid tumor. This may be a thyroid carcinoma. About 90% of carcinomas are a very aggressive; they invade the surrounding tissues and metastasize (spread), to other tissues, particularly the lungs. This has a poor prognosis. Surgery to remove the tumor a carcinoma is often very difficult, due to the spread of the tumor to the surrounding tissue, for example, into arteries, the esophagus, or the windpipe. It may be possible to reduce the size of the tumor, thus relieving symptoms and allowing time for other treatments to work. About 10% of thyroid tumors are benign; these often cause few symptoms.

In dogs treated for hypothyroidism (lack of thyroid hormone), hyperthyroidism may occur as a result of an overdose of the thyroid hormone replacement medication, levothyroxine; in this case treatment involves reducing the dose of levothyroxine. Dogs which display coprophagy, that is, which often eat feces, and which live in a household with a dog receiving levothyroxine treatment, may develop hyperthryoidism if they frequently eat the feces from the dog receiving levothyroxine treatment.

Hyperthyroidism may occur if a dog eats an excessive amount of thyroid gland tissue. This has occurred in dogs fed commercial dog food.

Treatment of a thyroid nodule depends on many things including size of the nodule, age of the patient, the type of thyroid cancer, and whether or not it has spread to other tissues in the body.

If the nodule is benign, patients may receive thyroxine therapy to suppress thyroid-stimulating hormone and should be reevaluated in 6 months. However, if the benign nodule is inhibiting the patient's normal functions of life; such as breathing, speaking, or swallowing, the thyroid may need to be removed.

Sometimes only part of the thyroid is removed in an attempt to avoid causing hypothyroidism. There's still a risk of hypothyroidism though, as the remaining thyroid tissue may not be able to produce enough hormones in the long-run.

If the nodule is malignant or has indeterminate cytologic features, it may require surgery. A thyroidectomy is a medium risk surgery that can result complications if not performed correctly. Problems with the voice, nerve or muscular damage, or bleeding from a lacerated blood vessel are rare but serious complications that may occur. After removing the thyroid, the patient must be supplied with a replacement hormone for the rest of their life. This is commonly a daily oral medication prescribed by their endocrinologist.

Radioactive iodine-131 is used in patients with papillary or follicular thyroid cancer for ablation of residual thyroid tissue after surgery and for the treatment of thyroid cancer. Patients with medullary, anaplastic, and most Hurthle cell cancers do not benefit from this therapy. External irradiation may be used when the cancer is unresectable, when it recurs after resection, or to relieve pain from bone metastasis.

The exact cause is unclear; however, it is believed to involve a combination of genetic and environmental factors. While a theoretical mechanism occurs by which stress could cause an aggravation of the autoimmune response that leads to Graves' disease, more robust clinical data are needed for a firm conclusion.

A genetic predisposition for Graves' disease is seen, with some people more prone to develop TSH receptor activating antibodies due to a genetic cause. Human leukocyte antigen DR (especially DR3) appears to play a role. To date, no clear genetic defect has been found to point to a single gene cause.

Genes believed to be involved include those for thyroglobulin, thyrotropin receptor, protein tyrosine phosphatase nonreceptor type 22, and cytotoxic T-lymphocyte–associated antigen 4, among others.

There are several causes of hyperthyroidism. Most often, the entire gland is overproducing thyroid hormone. Less commonly, a single nodule is responsible for the excess hormone secretion, called a "hot" nodule. Thyroiditis (inflammation of the thyroid) can also cause hyperthyroidism. Functional thyroid tissue producing an excess of thyroid hormone occurs in a number of clinical conditions.

The major causes in humans are:

- Graves' disease. An autoimmune disease (usually, the most common etiology with 50-80% worldwide, although this varies substantially with location- i.e., 47% in Switzerland (Horst et al., 1987) to 90% in the USA (Hamburger et al. 1981)). Thought to be due to varying levels of iodine in the diet. It is eight times more common in females than males and often occurs in young females, around 20 – 40 years of age.

- Toxic thyroid adenoma (the most common etiology in Switzerland, 53%, thought to be atypical due to a low level of dietary iodine in this country)

- Toxic multinodular goiter

High blood levels of thyroid hormones (most accurately termed hyperthyroxinemia) can occur for a number of other reasons:

- Inflammation of the thyroid is called thyroiditis. There are several different kinds of thyroiditis including Hashimoto's thyroiditis (Hypothyroidism immune-mediated), and subacute thyroiditis (de Quervain's). These may be "initially" associated with secretion of excess thyroid hormone but usually progress to gland dysfunction and, thus, to hormone deficiency and hypothyroidism.

- Oral consumption of excess thyroid hormone tablets is possible (surreptitious use of thyroid hormone), as is the rare event of consumption of ground beef contaminated with thyroid tissue, and thus thyroid hormone (termed "hamburger hyperthyroidism").

- Amiodarone, an antiarrhythmic drug, is structurally similar to thyroxine and may cause either under- or overactivity of the thyroid.

- Postpartum thyroiditis (PPT) occurs in about 7% of women during the year after they give birth. PPT typically has several phases, the first of which is hyperthyroidism. This form of hyperthyroidism usually corrects itself within weeks or months without the need for treatment.

- A struma ovarii is a rare form of monodermal teratoma that contains mostly thyroid tissue, which leads to hyperthyroidism.

- Excess iodine consumption notably from algae such as kelp.

Thyrotoxicosis can also occur after taking too much thyroid hormone in the form of supplements, such as levothyroxine (a phenomenon known as exogenous thyrotoxicosis, alimentary thyrotoxicosis, or occult factitial thyrotoxicosis).

Hypersecretion of thyroid stimulating hormone (TSH), which in turn is almost always caused by a pituitary adenoma, accounts for much less than 1 percent of hyperthyroidism cases.

Toxic multinodular goiter (also known as toxic nodular goiter, or Plummer's disease) is a multinodular goiter associated with hyperthyroidism.

It is a common cause of hyperthyroidism in which there is excess production of thyroid hormones from functionally autonomous thyroid nodules, which do not require stimulation from thyroid stimulating hormone (TSH).

Toxic multinodular goiter is the second most common cause of hyperthyroidism (after Graves' disease) in the developed world, whereas iodine deficiency is the most common cause of hypothyroidism in developing-world countries where the population is iodine-deficient. (Decreased iodine leads to decreased thyroid hormone.) However, iodine deficiency can cause goitre (thyroid enlargement); within a goitre, nodules can develop. Risk factors for toxic multinodular goiter include individuals over 60 years of age and being female.

Thyroid neoplasm is a neoplasm or tumor of the thyroid. It can be a benign tumor such as thyroid adenoma, or it can be a malignant neoplasm (thyroid cancer), such as papillary, follicular, medullary or anaplastic thyroid cancer. Most patients are 25 to 65 years of age when first diagnosed; women are more affected than men. The estimated number of new cases of thyroid cancer in the United States in 2010 is 44,670 compared to only 1,690 deaths. Of all thyroid nodules discovered, only about 5 percent are cancerous, and under 3 percent of those result in fatalities.

Colloid nodules, also known as adenomatous nodules or colloid nodular goiter are benign, noncancerous enlargement of thyroid tissue. Although they may grow large, and there may be more than one, they are not malignant and they will not spread beyond the thyroid gland. Colloid nodules are the most common kind of thyroid nodule.

Parathyroid adenoma can be associated with overexpression of the cyclin D1 gene.

Worldwide about one billion people are estimated to be iodine deficient; however, it is unknown how often this results in hypothyroidism. In large population-based studies in Western countries with sufficient dietary iodine, 0.3–0.4% of the population have overt hypothyroidism. A larger proportion, 4.3–8.5%, have subclinical hypothyroidism. Of people with subclinical hypothyroidism, 80% have a TSH level below the 10 mIU/l mark regarded as the threshold for treatment. Children with subclinical hypothyroidism often return to normal thyroid function, and a small proportion develops overt hypothyroidism (as predicted by evolving antibody and TSH levels, the presence of celiac disease, and the presence of a goiter).

Women are more likely to develop hypothyroidism than men. In population-based studies, women were seven times more likely than men to have TSH levels above 10 mU/l. 2–4% of people with subclinical hypothyroidism will progress to overt hypothyroidism each year. The risk is higher in those with antibodies against thyroid peroxidase. Subclinical hypothyroidism is estimated to affect approximately 2% of children; in adults, subclinical hypothyroidism is more common in the elderly, and in Caucasians. There is a much higher rate of thyroid disorders, the most common of which is hypothyroidism, in individuals with Down syndrome and Turner syndrome.

Very severe hypothyroidism and myxedema coma are rare, with it estimated to occur in 0.22 per million people a year. The majority of cases occur in women over 60 years of age, although it may happen in all age groups.

Most hypothyroidism is primary in nature. Central/secondary hypothyroidism affects 1:20,000 to 1:80,000 of the population, or about one out of every thousand people with hypothyroidism.

Almost all thyroid adenomas are follicular adenomas. Follicular adenomas can be described as "cold", "warm" or "hot" depending on their level of function. Histopathologically, follicular adenomas can be classified according to their cellular architecture and relative amounts of cellularity and colloid into the following types:

- Fetal (microfollicular) - these have the potential for microinvasion. These consist of small, closely packed follicles lined with epithelium.

- colloid (macrofollicular) - these do "not" have any potential for microinvasion

- embryonal (atypical) - have the potential for microinvasion.

- Hürthle cell adenoma (oxyphil or oncocytic tumor) - have the potential for microinvasion.

- Hyalinizing trabecular adenoma

Papillary adenomas are very rare.

Worldwide, the most common cause for goitre is iodine deficiency, usually seen in countries that do not use iodized salt. Selenium deficiency is also considered a contributing factor. In countries that use iodized salt, Hashimoto's thyroiditis is the most common cause. Goitre can also result from cyanide poisoning; this is particularly common in tropical countries where people eat the cyanide-rich cassava root as the staple food.

- Sarcoidosis

- Amyloidosis

- Hydatidiform mole

- Cysts

- Acromegaly

- Pendred syndrome