The initial phase of hyperthyroid symptoms occurs transiently about two to six months postpartum. Typical symptoms include irritability, nervousness, palpitations, and heat intolerance. Hormonal disturbances during this phase tend to occur with lower intensity compared with the hypothyroid phase. As a result, the hyperthyroid phase may pass undetected. The second phase of hypothyroid symptoms is also transient and can occur anytime within the three- to twelve-month period postpartum. Women in this phase experience low energy, poor memory, impaired concentration, carelessness, dry skin, cold intolerance, and general aches and pains. After one year postpartum, euthyroid function resumes. Any case with hypothyroid symptoms extending beyond one year postpartum is not considered postpartum thyroiditis.

Women who test positive for thyroid antibodies may be at increased risk of developing symptoms associated with postpartum depression than women without thyroid antibodies.

Postpartum thyroiditis is a phenomenon observed following pregnancy and may involve hyperthyroidism, hypothyroidism or the two sequentially. It affects about 5% of all women within a year after giving birth. The first phase is typically hyperthyroidism. Then, the thyroid either returns to normal or a woman develops hypothyroidism. Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring lifelong treatment.

Postpartum thyroiditis is believed to result from the modifications to the immune system necessary in pregnancy, and histologically is a subacute lymphocytic thyroiditis. The process is normally self-limiting, but when conventional antibodies are found there is a high chance of this proceeding to permanent hypothyroidism. Postpartum thyroiditis is a member of the group of thyroiditis conditions known as resolving thyroiditis.

There are many different signs and symptoms for thyroiditis, none of which are exclusively limited to this disease. Many of the signs imitate symptoms of other diseases, so thyroiditis can sometimes be difficult to diagnose. Common hypothyroid symptoms manifest when thyroid cell damage is slow and chronic, and may include fatigue, weight gain, feeling "fuzzy headed", depression, dry skin, and constipation. Other, rarer symptoms include swelling of the legs, vague aches and pains, decreased concentration and so on. When conditions become more severe, depending on the type of thyroiditis, one may start to see puffiness around the eyes, slowing of the heart rate, a drop in body temperature, or even incipient heart failure. On the other hand, if the thyroid cell damage is acute, the thyroid hormone within the gland leaks out into the bloodstream causing symptoms of thyrotoxicosis, which is similar to those of hyperthyroidism. These symptoms include weight loss, irritability, anxiety, insomnia, fast heart rate, and fatigue. Elevated levels of thyroid hormone in the bloodstream cause both conditions, but thyrotoxicosis is the term used with thyroiditis since the thyroid gland is not overactive, as in the case of hyperthyroidism.

The symptoms may vary depending on the thyroid function, i.e. hyperthyroidism or hypothyroidism. Hyperthyroidism can cause sweating, rapid heart rate, anxiety, tremors, fatigue, difficulty sleeping, sudden weight loss, and protruding eyes. Hypothyroidism can cause weight gain, fatigue, dry skin, hair loss, intolerance to cold, and constipation. The effects of this disease may be permanent but can sometimes be transient. Symptoms may come and go depending on whether the person receives treatment, and whether the treatment takes effect.

Autoimmune thyroiditis, (or Chronic Autoimmune thyroiditis), is a chronic disease in which the body interprets the thyroid glands and its hormone products T3, T4 and TSH as threats, therefore producing special antibodies that target the thyroid’s cells, thereby destroying it.

It may present with hypothyroidism or hyperthyroidism and with or without a goiter.

Thyroid disease in women is an autoimmune disease that affects the thyroid in women. This condition can have a profound effect during pregnancy and on the child. It also is called Hashimoto's thyroiditis (theye-royd-EYET-uhss). During pregnancy, the infant may be seriously affected and have a variety of birth defects. Many women with Hashimoto's disease develop an underactive thyroid. They may have mild or no symptoms at first, but symptoms tend to worsen over time. If a woman is pregnant and has symptoms of Hashimoto's disease, the clinician will do an exam and order one or more tests.

The thyroid is a small gland in the front of the neck. The thyroid makes hormones called T3 and T4 that regulate how the body uses energy. Thyroid hormone levels are controlled by the pituitary, which is a pea-sized gland in the brain. It makes thyroid stimulating hormone (TSH), which triggers the thyroid to make thyroid hormone.

In thyroid disease the immune system makes antibodies that damage thyroid cells and interfere with their ability to make thyroid hormone. Over time, thyroid damage can cause thyroid hormone levels to be too low. This is called an underactive thyroid or hypothyroidism (heye-poh-THEYE-royd-ism). An underactive thyroid causes every function of the body to slow down, such as heart rate, brain function, and the rate your body turns food into energy. Hashimoto's disease is the most common cause of an underactive thyroid. It is closely related to Graves' disease, another autoimmune disease affecting the thyroid.

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.

Thyroiditis is a group of disorders that all cause thyroidal inflammation. Forms of the disease are Hashimoto's thyroiditis, the most common cause of hypothyroidism in the US, postpartum thyroiditis, subacute thyroiditis, silent thyroiditis, drug-induced thyroiditis, radiation-induced thyroiditis, acute thyroiditis, and Riedel's thyroiditis.

Each different type of this disease has its own causes, clinical features, diagnoses, durations, resolutions, conditions and risks.

Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis and Hashimoto's disease, is an autoimmune disease in which the thyroid gland is gradually destroyed. Early on there may be no symptoms. Over time the thyroid may enlarge forming a painless goiter. Some people eventually develop hypothyroidism with its accompanying weight gain, feeling tired, constipation, depression, and general pains. After many years the thyroid typically shrinks in size. Potential complications include thyroid lymphoma.

Hashimoto's thyroiditis is thought to be due to a combination of genetic and environmental factors. Risk factors include a family history of the condition and having another autoimmune disease. Diagnosis is confirmed with blood tests for TSH, T4, and antithyroid antibodies. Other conditions that can produce similar symptoms include Graves’ disease and nontoxic nodular goiter.

Hashimoto's thyroiditis is typically treated with levothyroxine. If hypothyroidism is not present some may recommend no treatment while others may treat to try to reduce the size of the goiter. Those affected should avoid eating large amounts of iodine; however, sufficient iodine is required especially during pregnancy. Surgery is rarely required to treat the goiter.

Hashimoto's thyroiditis affects about 5% of the population at some point in their life. It typically begins between the ages of 30 and 50 and is much more common in women than men. Rates of disease appear to be increasing. It was first described by the Japanese physician Hakaru Hashimoto in 1912. In 1957 it was recognized as an autoimmune disorder.

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.

There are many symptoms that are attributed to Hashimoto's thyroiditis or Hashimoto's disease. The most common symptoms include the following: fatigue, weight gain, pale or puffy face, feeling cold, joint and muscle pain, constipation, dry and thinning hair, heavy menstrual flow or irregular periods, depression, panic disorder, a slowed heart rate, and problems getting pregnant and maintaining pregnancy.

Hashimoto’s disease is about seven times more common in women than in men. It can occur in teens and young women, but more commonly shows up in middle age, particularly for men. People who develop Hashimoto’s disease often have family members who have thyroid or other autoimmune diseases, and sometimes have other autoimmune diseases themselves.

The thyroid gland may become firm, large, and lobulated in Hashimoto's thyroiditis, but changes in the thyroid can also be nonpalpable. Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis rather than tissue hypertrophy. Physiologically, antibodies against thyroid peroxidase (TPO) (also called TPOAb) and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. Accordingly, the disease can be detected clinically by looking for these antibodies in the blood. It is also characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. A rare but serious complication is thyroid lymphoma, generally the B-cell type, non-Hodgkin lymphoma.

Symptoms of Ord's thyroiditis include symptoms of hypothyroidism and atrophy of the thyroid gland.

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.

Subacute thyroiditis is a form of thyroiditis that can be a cause of both thyrotoxicosis and hypothyroidism. It is uncommon and can affect individuals of both sexes and people of all ages. The most common form, subacute granulomatous, or de Quervain's, thyroiditis manifests as a sudden and painful enlargement of the thyroid gland accompanied with fever, malaise and muscle aches. Indirect evidence has implicated viral infection in the aetiology of subacute thyroiditis. This evidence is limited to preceding upper respiratory tract infection, elevated viral antibody levels, and both seasonal and geographical clustering of cases. There may be a genetic predisposition.

Nishihara and coworkers studied the clinical features of subacute thyroiditis in 852 mostly 40- to 50-year-old women in Japan. They noted seasonal clusters (summer to early autumn) and most subjects presented with neck pain. Fever and symptoms of thyrotoxicosis was present in two thirds of subjects. Upper respiratory tract infections in the month preceding presentation were reported in only 1 in 5 subjects. Recurrent episodes following resolution of the initial episode were rare, occurring in just 1.6% of cases. Laboratory markers for thyroid inflammation and dysfunction typically peaked within one week of onset of illness.

Types include:

- Subacute granulomatous thyroiditis (De Quervain thyroiditis)

- Subacute lymphocytic thyroiditis

- Postpartum thyroiditis

- Palpation thyroiditis

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.

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.

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 .

Hyperthyroidism occurs in about 0.2-0.4% of all pregnancies. Most cases are due to Graves’ disease although less common causes (e.g. toxic nodules and thyroiditis) may be seen. Clinical assessment alone may occasionally be inadequate in differentiating hyperthyroidism from the hyperdynamic state of pregnancy. Distinctive clinical features of Graves’ disease include the presence of ophthalmopathy, diffuse goitre and pretibial myxoedema. Also, hyperthyroidism must be distinguished from gestational transient thyrotoxicosis, a self-limiting hyperthyroid state due to the thyroid stimulatory effects of beta-hCG . This distinction is important since the latter condition is typically mild and will not usually require specific antithyroid treatment. Red cell zinc may also be useful in differentiating the two. Hyperthyroidism due to Graves’ disease may worsen in the first trimester of pregnancy, remit in later pregnancy, and subsequently relapse in the postpartum.

Ord's thyroiditis is a common form of thyroiditis, an autoimmune disease where the body's own antibodies fight the cells of the thyroid.

It is named after the physician, William Miller Ord, who first described it in 1877 and again in 1888.

It is more common among women than men.

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%.

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.

Experts have not reached agreement on whether all pregnant women should be routinely screened for thyroid problems. But, if an underactive thyroid with or without symptoms is found during pregnancy it will be treated to lower the risk of pregnancy problems. An underactive thyroid without symptoms occurs in 2 to 3 in every 100 pregnancies. Women can request thyroid screening.

Hashitoxicosis, which can be abbreviated "Htx", is a transient hyperthyroidism caused by inflammation associated with Hashimoto's thyroiditis disturbing the thyroid follicles, resulting in excess release of thyroid hormone.

Major clinical signs include weight loss (often accompanied by an increased appetite), anxiety, intolerance to heat, fatigue, hair loss, weakness, hyperactivity, irritability, apathy, depression, polyuria, polydipsia, delirium, and sweating. Additionally, patients may present with a variety of symptoms such as palpitations and

arrhythmias (notably atrial fibrillation), shortness of breath (dyspnea), loss of libido, nausea, vomiting, and diarrhea. Long term untreated hyperthyroidism can lead to osteoporosis. In the elderly, these classical symptoms may not be present.

Myxedema can occur in the lower leg (pretibial myxedema) and behind the eyes (exophthalmos).