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.

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%.

Thyrotoxicosis factitia refers to a condition of thyrotoxicosis caused by the ingestion of exogenous thyroid hormone. It can be the result of mistaken ingestion of excess drug, such as levothyroxine, or as a symptom of Munchausen syndrome. It is an uncommon form of hyperthyroidism.

Patients present with hyperthyroidism and may be mistaken for Graves’ disease, if TSH receptor positive, or thyroiditis because of absent uptake on a thyroid radionuclide uptake scan due to suppression of thyroid function by exogenous thyroid hormones. Ingestion of thyroid hormone also suppresses thyroglobulin levels helping to differentiate thyrotoxicosis factitia from other causes of hyperthyroidism, in which serum thyroglobulin is elevated. Caution, however, should be exercised in interpreting thyroglobulin results without thyroglobulin antibodies, since thyroglobulin antibodies commonly interfere in thyroglobulin immunoassays causing false positive and negative results which may lead to clinical misdirection. In such cases, increased faecal thyroxine levels in thyrotoxicosis factitia may help differentiate it from other causes of hyperthyroidism.

Thyroid storm is characterized by an acute onset of symptoms of hyperthyroidism (fast heart rate, restlessness, agitation) accompanied by other features such as fever (temperatures often above 40 °C/104 °F), mental status changes, diarrhea, and vomiting.

Individuals can exhibit varying signs of organ dysfunction. Patients may experience liver dysfunction, and yellow discoloration of the skin is considered a poor prognostic sign. Heart (cardiac) symptoms include abnormal heart rhythms, decreased blood flow to the heart and heart attacks, and congestive heart failure, which may lead to cardiovascular collapse. Mortality can be as high as 20-30%.

In some situations, individuals may not experience the classic signs of restlessness and agitation, but instead present with apathetic signs of weakness and confusion.

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.

The transition from hyperthyroidism to thyroid storm is typically triggered by a non-thyroidal insult including, but not limited to fever, sepsis, dehydration, myocardial infarction, and psychiatric diseases. Individuals are at higher risk of thyroid storm if their hyperthyroidism is incompletely treated or if their anti-thyroid drugs are discontinued. Many of these individuals have underlying primary causes of hyperthyroidism (Graves disease, toxic multi-nodular goiter, solitary toxic adenoma). However, thyroid storm can occur in individuals with unrecognized thyrotoxicosis experiencing non-thyroid surgery, labor, infection, or exposure to certain medications and radiocontrast dyes.

Thyroid-associated ophthalmopathy (TAO), or thyroid eye disease (TED), is the most common extrathyroidal manifestation of Grave's disease. It is a form of idiopathic lymphocytic orbital inflammation, and although its pathogenesis is not completely understood, autoimmune activation of orbital fibroblasts, which in TAO express the TSH receptor, is thought to play a central role.

Hypertrophy of the extraocular muscles, adipogenesis, and deposition of nonsulfated glycoaminoglycans and hyaluronate, causes expansion of the orbital fat and muscle compartments, which within the confines of the bony orbit may lead to dysthyroid optic neuropathy, increased intraocular pressures, proptosis, venous congestion leading to chemosis and periorbital edema, and progressive remodeling of the orbital walls. Other distinctive features of TAO include lid retraction, restrictive myopathy, superior limbic keratoconjunctivitis, and exposure keratopathy.

Severity of eye disease may be classified by the mnemonic: "NO SPECS":

- Class 0: No signs or symptoms

- Class 1: Only signs (limited to upper lid retraction and stare, with or without lid lag)

- Class 2: Soft tissue involvement (oedema of conjunctivae and lids, conjunctival injection, etc.)

- Class 3: Proptosis

- Class 4: Extraocular muscle involvement (usually with diplopia)

- Class 5: Corneal involvement (primarily due to lagophthalmos)

- Class 6: Sight loss (due to optic nerve involvement)

Typically the natural history of TAO follows Rundle's curve, which describes a rapid worsening during an initial phase, up to a peak of maximum severity, and then improvement to a static plateau without, however, resolving back to a normal condition.

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.

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.

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.

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.

Uncontrolled hyperthyroidism in pregnancy is associated with an increased risk of severe pre-eclampsia and up to a four-fold increased risk of low birth weight deliveries. Some of these unfavourable outcomes are more marked in women who are diagnosed for the first time in pregnancy. A recent study has also shown that already high normal maternal FT4 levels are associated with a decrease in child IQ and gray matter and cortex volumes, similar to the effects of hypothyroidism.

Uncontrolled and inadequately treated maternal hyperthyroidism may also result in fetal and neonatal hyperthyroidism due to the transplacental transfer of stimulatory TSH receptor antibodies (TRAbs). Clinical neonatal hyperthyroidism occurs in about 1% of infants born to mothers with Graves’ disease. Rarely neonatal hypothyroidism may also be observed in the infants of mothers with Graves’ hyperthyroidism. This may result from transplacental transfer of circulating maternal anti-thyroid drugs, pituitary-thyroid axis suppression from transfer of maternal thyroxine.

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.

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.

Euthyroid sick syndrome (ESS), sick euthyroid syndrome (SES), thyroid allostasis in critical illness, tumours, uremia and starvation (TACITUS), non-thyroidal illness syndrome (NTIS) or low T low T syndrome is a state of adaptation or dysregulation of thyrotropic feedback control where the levels of T3 and/or T4 are at unusual levels, but the thyroid gland does not appear to be dysfunctional.

This condition is often seen in starvation, critical illness or patients in intensive care unit. Similar endocrine phenotypes are observed in fetal life and in hibernating mammals The most common hormone pattern in sick euthyroid syndrome is a low total and unbound T3 levels with normal T4 and TSH levels.

Causes of euthyroid sick syndrome include a number of acute and chronic conditions, including pneumonia, fasting, starvation, anorexia nervosa, sepsis, trauma, cardiopulmonary bypass, malignancy, stress, heart failure, hypothermia, myocardial infarction, chronic renal failure, cirrhosis, and diabetic ketoacidosis.

Euthyroid sick syndrome (non-thyroidal illness syndrome) has been assumed closely related with a series of diseases, (such as inflammatory bowel disease).

An attack often begins with muscle pain, cramping, and stiffness. This is followed by weakness or paralysis that tends to develop rapidly, usually in late evening or the early hours of the morning. The weakness is usually symmetrical; the limb muscles closer to the trunk (proximal) are predominantly affected, and weakness tends to start in the legs and spread to the arms. Muscles of the mouth and throat, eyes, and breathing are usually not affected, but occasionally weakness of the respiratory muscles can cause life-threatening respiratory failure. Attacks typically resolve within several hours to several days, even in the absence of treatment. On neurological examination during an attack, flaccid weakness of the limbs is noted; reflexes are usually diminished, but the sensory system is unaffected. Mental status is not affected.

Attacks may be brought on by physical exertion, drinking alcohol, or eating food high in carbohydrates or salt. This may explain why attacks are more common in summer, when more people drink sugary drinks and engage in exercise. Exercise-related attacks tend to occur during a period of rest immediately after exercise; exercise may therefore be recommended to abort an attack.

There may be symptoms of thyroid overactivity, such as weight loss, a fast heart rate, tremor, and perspiration; but such symptoms occur in only half of all cases. The most common type of hyperthyroidism, Graves' disease, may additionally cause eye problems (Graves' ophthalmopathy) and skin changes of the legs (pretibial myxedema). Thyroid disease may also cause muscle weakness in the form of thyrotoxic myopathy, but this is constant rather than episodic.

Thyrotoxic periodic paralysis (TPP) is a condition featuring attacks of muscle weakness in the presence of hyperthyroidism (overactivity of the thyroid gland). Hypokalemia (a decreased potassium level in the blood) is usually present during attacks. The condition may be life-threatening if weakness of the breathing muscles leads to respiratory failure, or if the low potassium levels lead to cardiac arrhythmias (irregularities in the heart rate). If untreated, it is typically recurrent in nature.

The condition has been linked with genetic mutations in genes that code for certain ion channels that transport electrolytes (sodium and potassium) across cell membranes. The main ones are the L-type calcium channel α1-subunit and potassium inward rectifier 2.6; it is therefore classified as a channelopathy. The abnormality in the channel is thought to lead to shifts of potassium into cells, under conditions of high thyroxine (thyroid hormone) levels, usually with an additional precipitant.

Treatment of the hypokalemia, followed by correction of the hyperthyroidism, leads to complete resolution of the attacks. It occurs predominantly in males of Chinese, Japanese, Vietnamese, Filipino, and Korean descent. TPP is one of several conditions that can cause periodic paralysis.

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.

Acropachy or thyroid acropachy refers to a dermopathy associated with Graves' disease. It is characterized by soft-tissue swelling of the hands and clubbing of the fingers. Radiographic imaging of affected extremities typically demonstrates periostitis, most commonly the metacarpal bones. The exact cause is unknown, but it is thought to be caused by stimulating auto-antibodies that are implicated in the pathophysiology of Graves' thyrotoxicosis. There is no effective treatment for acropachy.

Since it is closely associated with Graves' disease, it is associated with other manifestations of Graves' disease, such as Graves' ophthalmopathy and thyroid dermopathy.

Hereditary acropachy (also known as "isolated congenital nail clubbing") may be associated with HPGD.

In the initial phase of damage to the gland, preformed thyroid hormone will 'fall out' of the damaged cells. This leads to symptoms and biochemistry of an overactive thyroid (feels hot, trembly, anxious, loses weight, fast heart rate, sweaty, greasy hair), with raised free T3 and free T4, and a suppressed thyroid stimulating hormone (TSH) value. The damaged cells will no longer be able to take up iodine in order to manufacture further supplies of thyroid hormone, and thus in due course the patient comes to experience the symptoms of an underactive thyroid (feels cold, tired, depressed, gains weight, dry skin and hair) with low free T3 and free T4, and eventually increased TSH.

With the standard overactive thyroid, iodine uptake into the thyroid is avid, whereas if the cells are damaged, then uptake is poor. In this way, if there is doubt about whether the patient has too much thyroid hormone because of de Quervain's thyroiditis, then measuring radio-iodine uptake or technetium uptake gives a clear cut answer as it will be higher than normal in standard thyrotoxicosis and lower than normal in de Quervain's.

Infiltrative ophthalmopathy is found in 5-10% of patients with Graves disease and resembles exophthalmos, except that the blurry or double vision is acquired because of weakness in the ocular muscles of the eye. In addition, there is no known correlation with the patient's thyroid levels. Exophthalmos associated with Grave's disease disappears when the thyrotoxicosis is corrected. Infiltrative ophthalmopathy at times may not be cured. Treatments consist of high dose glucocorticoids and low dose radiotherapy. The current hypothesis is that infiltrative ophthalmopathy may be autoimmune in nature targeting retrobulbar tissue. Smoking may also have a causative effect.

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

Three common descriptions of "palpitation" are "flip-flopping" (or "stop and start"), often caused by premature contraction of the atrium or ventricle, with the perceived "stop" from the pause following the contraction, and the "start" from the subsequent forceful contraction; rapid "fluttering in the chest," with regular "fluttering" suggesting supraventricular or ventricular arrhythmias (including sinus tachycardia) and irregular "fluttering" suggesting atrial fibrillation, atrial flutter, or tachycardia with variable block; and "pounding in the neck" or neck pulsations, often due to "cannon" A waves in the jugular venous pulsations that occur when the right atrium contracts against a closed tricuspid valve.

Palpitation associated with chest pain suggests coronary artery disease, or if the chest pain is relieved by leaning forward, pericardial disease is suspected. Palpitation associated with light-headedness, fainting or near fainting suggest low blood pressure and may signify a life-threatening abnormal heart rhythm. Palpitation that occurs regularly with exertion suggests a rate-dependent bypass tract or hypertrophic cardiomyopathy. If a benign cause for these concerning symptoms cannot be found at the initial visit, then ambulatory monitoring or prolonged heart monitoring in the hospital might be warranted. Noncardiac symptoms should also be elicited since the palpitations may be caused by a normal heart responding to a metabolic or inflammatory condition. Weight loss suggests hyperthyroidism. Palpitation can be precipitated by vomiting or diarrhea that leads to electrolyte disorders and hypovolemia. Hyperventilation, hand tingling, and nervousness are common when anxiety or panic disorder is the cause of the palpitations.

It is associated with various physiological as well as pathological changes, or may be a normal finding:

- Portal hypertension

- Chronic liver disease (including chronic hepatitis)

- Pregnancy

- Polycythemia

- Thyrotoxicosis

- Rheumatoid arthritis (especially in patients with polycythaemia)

- Eczema and psoriasis

- Deep telangiectasias

- Coxsackievirus A infection (Hand, foot and mouth disease)

- Rocky Mountain spotted fever

- Secondary syphilis

- Kawasaki disease

- Adverse drug reaction: palmoplantar erythrodysesthesia (acral erythema)

Because circulating levels of estrogen increase in both cirrhosis and pregnancy, estrogen was thought to be the cause for the increased vascularity. More recently, nitric oxide has been implicated in the pathogenesis of palmar erythema.