Nontoxic nodular goiter is an enlarged thyroid without hyperthyroidism. It is often present for years before toxic nodular goiter occurs. In the United States it is the most common cause of a large thyroid affecting between 3 and 5% of the population.

Often these abnormal growths of thyroid tissue are located at the edge of the thyroid gland and can be felt as a lump in the throat. When they are large, they can sometimes be seen as a lump in the front of the neck.

Sometimes a thyroid nodule presents as a fluid-filled cavity called a thyroid cyst. Often, solid components are mixed with the fluid. Thyroid cysts most commonly result from degenerating thyroid adenomas, which are benign, but they occasionally contain malignant solid components.

Symptoms of toxic multinodular goitre are similar to that of hyperthyroidism, including:

- heat intolerance

- muscle weakness/wasting

- hyperactivity

- fatigue

- tremor

- irritability

- weight loss

- osteoporosis

- increased appetite

- non-painful goitre (swelling of the thyroid gland)

- tachycardia (high heart rate - above 100 beats per minute at rest in adults)

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.

Colloid nodules are usually small enough to be undetectable without an ultrasound or other imaging techniques. They usually produce no symptoms, so patients are unlikely to notice them until their size makes them easier to detect. Like other thyroid nodules, they are usually first noticed in a routine physical examination.

Thyroid nodules are nodules (raised areas of tissue or fluid) which commonly arise within an otherwise normal thyroid gland. They may be hyperplasia or a thyroid neoplasm, but only a small percentage of the latter are thyroid cancers. Small, asymptomatic nodules are common, and many people who have them are unaware of them. But nodules that grow larger or produce symptoms may eventually need medical care. Goitres may have nodules or be diffuse.

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".

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.

Symptoms of the condition vary with type: hypo- vs. hyperthyroidism, which are further described below.

Possible symptoms of hypothyroidism are:

Possible symptoms of hyperthyroidism are:Note: certain symptoms and physical changes can be seen in both hypothyroidism and hyperthyroidism —fatigue, fine / thinning hair, menstrual cycle irregularities, muscle weakness / aches (myalgia), and different forms of myxedema.

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.

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.

Thyroid disease is a medical condition that affects the function of the thyroid gland (the endocrine organ found at the front of the neck that produces thyroid hormones). The symptoms of thyroid disease vary depending on the type. There are four general types: 1) hypothyroidism (low function) caused by not having enough thyroid hormones; 2) hyperthyroidism (high function) caused by having too much thyroid hormones; 3) structural abnormalities, most commonly an enlargement of the thyroid gland; and 4) tumors which can be benign or cancerous. It is also possible to have abnormal thyroid function tests without any clinical symptoms. Common hypothyroid symptoms include fatigue, low energy, weight gain, inability to tolerate the cold, slow heart rate, dry skin and constipation. Common hyperthyroid symptoms include irritability, weight loss, fast heartbeat, heat intolerance, diarrhea, and enlargement of the thyroid. In both hypothyroidism and hyperthyroidism, there may be swelling of a part of the neck, which is also known as goiter.

Diagnosis can often be made through laboratory tests. The first is thyroid-stimulating hormone (TSH), which is generally below normal in hyperthyroidism and above normal in hypothyroidism. The other useful laboratory test is non-protein-bound thyroxine or free T4. Total and free triiodothyronine (T3) levels are less commonly used. Anti-thyroid autoantibodies can also be used, where elevated anti-thyroglobulin and anti-thyroid peroxidase antibodies are commonly found in hypothyroidism from Hashimoto's thyroiditis and TSH-receptor antibodies are found in hyperthyroidism caused by Graves' disease. Procedures such as ultrasound, biopsy and a radioiodine scanning and uptake study may also be used to help with the diagnosis.

Treatment of thyroid disease varies based on the disorder. Levothyroxine is the mainstay of treatment for people with hypothyroidism, while people with hyperthyroidism caused by Graves' disease can be managed with iodine therapy, antithyroid medication, or surgical removal of the thyroid gland. Thyroid surgery may also be performed to remove a thyroid nodule or lobe for biopsy, or if there is a goiter that is unsightly or obstructs nearby structures.

Hypothyroidism affects 3-10% percent of adults, with a higher incidence in women and the elderly. An estimated one-third of the world's population currently lives in areas of low dietary iodine levels, making iodine-deficiency the most common cause of hypothyroidism and endemic goiter. In regions of severe iodine deficiency, the prevalence of goiter is as high as 80%. In areas where iodine-deficiency is not found, the most common type of hypothyroidism is an autoimmune subtype called Hashimoto's thyroiditis, with a prevalence of 1-2%. As for hyperthyroidism, Graves' disease, another autoimmune condition, is the most common type with a prevalence of 0.5% in males and 3% in females. Although thyroid nodules are common, thyroid cancer is rare. Thyroid cancer accounts for less than 1% of all cancer in the UK, though it is the most common endocrine tumor and makes up greater than 90% of all cancers of the endocrine glands.

The signs and symptoms of Graves' disease virtually all result from the direct and indirect effects of hyperthyroidism, with main exceptions being Graves' ophthalmopathy, goiter, and pretibial myxedema (which are caused by the autoimmune processes of the disease). Symptoms of the resultant hyperthyroidism are mainly insomnia, hand tremor, hyperactivity, hair loss, excessive sweating, shaking hands, itching, heat intolerance, weight loss despite increased appetite, diarrhea, frequent defecation, palpitations, muscle weakness, and skin warmth and moistness. Further signs that may be seen on physical examination are most commonly a diffusely enlarged (usually symmetric), nontender thyroid, lid lag, excessive lacrimation due to Graves' ophthalmopathy, arrhythmias of the heart, such as sinus tachycardia, atrial fibrillation, and premature ventricular contractions, and hypertension. People with hyperthyroidism may experience behavioral and personality changes, including: psychosis, mania, anxiety, agitation, and depression.

Patients will experience a hyperthyroid period as the cellular lining of colloid spaces fails, allowing abundant colloid into the circulation, with neck pain and fever. Patients typically then become hypothyroid as the pituitary reduces TSH production and the inappropriately released colloid is depleted before resolving to euthyroid. The symptoms are those of hyperthyroidism and hypothyroidism. In addition, patients may suffer from painful dysphagia. There are multi-nucleated giant cells on histology. Thyroid antibodies can be present in some cases. The clinical presentation during the hyperthyroid phase can mimic those of Diffuse Toxic Goiter or Graves' disease. In such cases, a radionuclide thyroid uptake and scan can be helpful, since subacute thyroiditis will result in decreased isotope uptake, while Graves' disease will generally result in increased uptake. Distinguishing between these two types of disease is important, since Graves' disease and Diffuse Toxic Goiter can be treated with radioiodine therapy, but subacute thyroiditis is usually self-limited and is not treated with radioiodine.

Thyroid storm is a severe form of thyrotoxicosis characterized by rapid and often irregular heart beat, high temperature, vomiting, diarrhea, and mental agitation. Symptoms may be unusual in the young, old, or pregnant. It is a medical emergency and requires hospital care to control the symptoms rapidly. Even with treatment, death occurs in 20% to 50%.

Subacute lymphocytic thyroiditis features a small goiter without tenderness. This condition tends to have a phase of hyperthyroidism followed by a return to a euthyroid state, and then a phase of hypothyroidism, followed again by a return to the euthyroid state. The time span of each phase can vary; however, each phase usually lasts 2–3 months.

A thyroid adenoma is distinguished from a multinodular goiter of the thyroid in that an adenoma is typically solitary, and is a neoplasm resulting from a genetic mutation (or other genetic abnormality) in a single precursor cell. In contrast, a multinodular goiter is usually thought to result from a hyperplastic response of the entire thyroid gland to a stimulus, such as iodine deficiency.

Careful pathological examination may be necessary to distinguish a thyroid adenoma from a minimally invasive follicular thyroid carcinoma.

People with hypothyroidism often have no or only mild symptoms. Numerous symptoms and signs are associated with hypothyroidism, and can be related to the underlying cause, or a direct effect of having not enough thyroid hormones. Hashimoto's thyroiditis may present with the mass effect of a goiter (enlarged thyroid gland).

Delayed relaxation after testing the ankle jerk reflex is a characteristic sign of hypothyroidism and is associated with the severity of the hormone deficit.

Myxedema coma is a rare but life-threatening state of extreme hypothyroidism. It may occur in those who are known to have hypothyroidism when they develop another illness, but it can be the first presentation of hypothyroidism. The illness is characterized by very low body temperature without shivering, confusion, a slow heart rate and reduced breathing effort. There may be physical signs suggestive of hypothyroidism, such as skin changes or enlargement of the tongue.

Hyperthyroidism may be asymptomatic or present with significant symptoms. Some of the symptoms of hyperthyroidism include nervousness, irritability, increased perspiration, heart racing, hand tremors, anxiety, difficulty sleeping, thinning of the skin, fine brittle hair, and muscular weakness—especially in the upper arms and thighs. More frequent bowel movements may occur, and diarrhea is common. Weight loss, sometimes significant, may occur despite a good appetite (though 10% of people with a hyperactive thyroid experience weight gain), vomiting may occur, and, for women, menstrual flow may lighten and menstrual periods may occur less often, or with longer cycles than usual.

Thyroid hormone is critical to normal function of cells. In excess, it both overstimulates metabolism and exacerbates the effect of the sympathetic nervous system, causing "speeding up" of various body systems and symptoms resembling an overdose of epinephrine (adrenaline). These include fast heart beat and symptoms of palpitations, nervous system tremor such as of the hands and anxiety symptoms, digestive system hypermotility, unintended weight loss, and (in "lipid panel" blood tests) a lower and sometimes unusually low serum cholesterol.

Major clinical signs include weight loss (often accompanied by an increased appetite), anxiety, heat intolerance, hair loss (especially of the outer third of the eyebrows), muscle aches, weakness, fatigue, hyperactivity, irritability, high blood sugar, excessive urination, excessive thirst, delirium, tremor, pretibial myxedema (in Graves' disease), emotional lability, and sweating. Panic attacks, inability to concentrate, and memory problems may also occur. Psychosis and paranoia, common during thyroid storm, are rare with milder hyperthyroidism. Many persons will experience complete remission of symptoms 1 to 2 months after a euthyroid state is obtained, with a marked reduction in anxiety, sense of exhaustion, irritability, and depression. Some individuals may have an increased rate of anxiety or persistence of affective and cognitive symptoms for several months to up to 10 years after a euthyroid state is established. In addition, those with hyperthyroidism may present with a variety of physical symptoms such as palpitations and abnormal heart rhythms (the notable ones being atrial fibrillation), shortness of breath (dyspnea), loss of libido, amenorrhea, nausea, vomiting, diarrhea, gynecomastia and feminization. Long term untreated hyperthyroidism can lead to osteoporosis. These classical symptoms may not be present often in the elderly.

Neurological manifestations can include tremors, chorea, myopathy, and in some susceptible individuals (in particular of Asian descent) periodic paralysis. An association between thyroid disease and myasthenia gravis has been recognized. The thyroid disease, in this condition, is autoimmune in nature and approximately 5% of patients with myasthenia gravis also have hyperthyroidism. Myasthenia gravis rarely improves after thyroid treatment and the relationship between the two entities is not well understood.

In Graves' disease, ophthalmopathy may cause the eyes to look enlarged because the eye muscles swell and push the eye forward. Sometimes, one or both eyes may bulge. Some have swelling of the front of the neck from an enlarged thyroid gland (a goiter).

Minor ocular (eye) signs, which may be present in any type of hyperthyroidism, are eyelid retraction ("stare"), extraocular muscle weakness, and lid-lag. In hyperthyroid "stare" (Dalrymple sign) the eyelids are retracted upward more than normal (the normal position is at the superior corneoscleral limbus, where the "white" of the eye begins at the upper border of the iris). Extraocular muscle weakness may present with double vision. In lid-lag (von Graefe's sign), when the patient tracks an object downward with their eyes, the eyelid fails to follow the downward moving iris, and the same type of upper globe exposure which is seen with lid retraction occurs, temporarily. These signs disappear with treatment of the hyperthyroidism.

Neither of these ocular signs should be confused with exophthalmos (protrusion of the eyeball), which occurs specifically and uniquely in hyperthyroidism caused by Graves' disease (note that not all exophthalmos is caused by Graves' disease, but when present with hyperthyroidism is diagnostic of Graves' disease). This forward protrusion of the eyes is due to immune-mediated inflammation in the retro-orbital (eye socket) fat. Exophthalmos, when present, may exacerbate hyperthyroid lid-lag and stare.

One particular familial form is associated with sensorineural deafness (Pendred's syndrome).

OMIM includes the following:

Some specific reactive lymphadenopathies with a predominantly follicular pattern:

- Rheumatoid arthritis

- Sjogren syndrome

- IgG4-related disease (IgG4-related lymphadenopathy)

- Kimura disease

- Toxoplasmosis

- Syphilis

- Castleman disease

- HIV-associated lymphadenopathy

- Progressive transformation of germinal centers (PTGC)

Some cases may be viral in origin, perhaps preceded by an upper respiratory tract infection. Viral causes include Coxsackie virus, mumps and adenoviruses. Some cases develop postpartum .

Subacute lymphocytic thyroiditis is a form of thyroiditis that is also known as silent thyroiditis or painless thyroiditis. Subacute lymphocytic thyroiditis may occur at any age and is more common in females.

A variant of subacute lymphocytic thyroiditis occurs postpartum, postpartum thyroiditis. Both of these entities can be considered subtypes of Hashimoto's thyroiditis and have an autoimmune basis. Anti-thyroid antibodies are common in all three and the underlying histology is similar. This disorder should not be confused with de Quervain's thyroiditis which is another form of subacute thyroiditis.

Graves' disease, also known as toxic diffuse goiter, is an autoimmune disease that affects the thyroid. It frequently results in and is the most common cause of hyperthyroidism. It also often results in an enlarged thyroid. Signs and symptoms of hyperthyroidism may include irritability, muscle weakness, sleeping problems, a fast heartbeat, poor tolerance of heat, diarrhea, and unintentional weight loss. Other symptoms may include thickening of the skin on the shins, known as pretibial myxedema, and eye bulging, a condition caused by Graves' ophthalmopathy. About 25 to 80% of people with the condition develop eye problems.

The exact cause is unclear; however, it is believed to involve a combination of genetic and environmental factors. A person is more likely to be affected if they have a family member with the disease. If one twin is affected, a 30% chance exists that the other twin will also have the disease. The onset of disease may be triggered by stress, infection, or giving birth. Those with other autoimmune diseases such as type 1 diabetes and rheumatoid arthritis are more likely to be affected. Smoking increases the risk of disease and may worsen eye problems. The disorder results from an antibody, called thyroid stimulating immunoglobulin (TSI), that has a similar effect to thyroid stimulating hormone (TSH). These TSI antibodies cause the thyroid gland to produce excess thyroid hormone. The diagnosis may be suspected based on symptoms and confirmed with blood tests and radioiodine uptake. Typically, blood tests show a raised T and T, low TSH, increased radioiodine uptake in all areas of the thyroid, and TSI antibodies.

The three treatment options are radioiodine therapy, medications, and thyroid surgery. Radioiodine therapy involves taking iodine-131 by mouth, which is then concentrated in the thyroid and destroys it over weeks to months. The resulting hypothyroidism is treated with synthetic thyroid hormone. Medications such as beta blockers may control some of the symptoms, and antithyroid medications such as methimazole may temporarily help people while other treatments are having effect. Surgery to remove the thyroid is another option. Eye problems may require additional treatments.

Graves' disease will develop in about 0.5% of males and 3% of females. It occurs about 7.5 times more often in women than men. Often, it starts between the ages of 40 and 60, but can begin at any age. It is the most common cause of hyperthyroidism in the United States (about 50 to 80% of cases). The condition is named after Robert Graves, who described it in 1835. A number of prior descriptions also exist.