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Also called: Overactive thyroid Hyperthyroidism, or overactive thyroid, happens when your thyroid gland makes more thyroid hormones than your body needs. Your thyroid is a small, butterfly-shaped gland in the front of your neck. It makes hormones that control the way the body uses energy. These hormones affect nearly every organ in your body and control many of your body's most important functions. For example, they affect your breathing, heart rate, weight, digestion, and moods. If not treated, hyperthyroidism can cause serious problems with your heart, bones, muscles, menstrual cycle, and fertility. But there are treatments that can help. Hyperthyroidism has several causes. They include: You are at higher risk for hyperthyroidism if you: The symptoms of hyperthyroidism can vary from person to person and may include: Adults over age 60 may have different symptoms than younger adults. For example, they may lose their appetite or withdraw from other people. Sometimes this can be mistaken for depression or dementia. If hyperthyroidism isn't treated, it can cause some serious health problems, including: Your health care provider may use many tools to make a diagnosis: The treatments for hyperthyroidism include medicines, radioiodine therapy, and thyroid surgery: If you have hyperthyroidism, it's important not to get too much iodine. Talk to your health care provider about which foods, supplements, and medicines you need to avoid. NIH: National Institute of Diabetes and Digestive and Kidney Diseases
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Thyrotoxicosis is the clinical manifestation of excess thyroid hormone action at the tissue level due to inappropriately high circulating thyroid hormone concentrations. Hyperthyroidism is a subset of thyrotoxicosis, referring specifically to excess thyroid hormone synthesis and secretion by the thyroid gland. The most common cause of thyrotoxicosis is Graves’ disease, an autoimmune condition that results in excess endogenous production of thyroid hormones.1 You might also be interested in our medical flashcard collection which contains over 1000 flashcards that cover key medical topics. AetiologyAnatomyThe thyroid gland is located within the neck at the level of the C5-T1 vertebrae. It consists of a central isthmus and two lobes, to the left and the right. The gland sits anterior to the trachea with the four parathyroid glands, which sit on the posterior surface of the thyroid gland.2 PhysiologyThyroid hormones are produced from follicular cells of the thyroid gland. Production of these hormones is regulated via the hypothalamic-pituitary-thyroid (HPT) axis (Figure 1). Thyrotropin-releasing hormone (TRH) is released from the paraventricular nucleus of the hypothalamus. TRH binds to pituitary receptors and causes the production of thyroid-stimulating hormone (TSH) from pituitary cells known as thyrotrophs. TSH subsequently binds to receptors on the thyroid gland and causes the production of thyroid hormones from the thyroid follicular cells. These hormones are triiodothyronine (T3) and thyroxine (T4). The HPT axis is regulated via negative feedback, at the level of the hypothalamus and the pituitary. Excess concentrations of thyroid hormones feedback to both the hypothalamus and the pituitary to cause a reduction in both TRH and TSH production. This decreases the rate of thyroid hormone production via the HPT axis. This physiological regulation of the HPT axis is lost in thyrotoxicosis.3 T4 is the main hormone produced from the thyroid gland, alongside smaller amounts of T3. The majority of T4 is then converted to T3 when it reaches the target tissue (this is the most active form of the hormone).4 Thyroid hormones have a wide range of functions including influencing the basal metabolic rate (the rate of cellular oxidative phosphorylation). Increased thyroid hormone concentration (seen in thyrotoxicosis) increases the basal metabolic rate. Thyroid hormones also have a key role in physiological growth, including fetal growth (thyroid hormones mediate the growth of neuronal and dendritic cells within the fetal central nervous system) and paediatric growth (thyroid hormones stimulate the expression of the pituitary growth hormone).5 Figure 1. The hypothalamic-pituitary-thyroid (HPT) axisCauses of thyrotoxicosisGraves’ diseaseGraves’ disease is the most common cause of thyrotoxicosis and hyperthyroidism. This is an autoimmune condition mediated via anti-TSH-Receptor (anti-TSHR) autoantibodies. These autoantibodies bind to TSH-receptors on the thyroid gland and stimulate increased production of T3 and T4 from the thyroid gland, resulting in thyrotoxicosis. Thyroxine receptors in the pituitary gland are activated by the excess hormone, resulting in the suppression of TSH release due to negative feedback. The result is very high levels of circulating thyroid hormones and a low TSH level. The prevalence of Graves’ disease in the UK is 0.5%, typically presenting in patients between the ages of 40 and 60, and is much more common in female patients. Graves’ disease is also strongly associated with other auto-immune conditions including type 1 diabetes mellitus, Addison’s disease and vitiligo.4 Toxic multinodular goitreToxic multinodular goitre (TMG) is caused by the development of physiologically active nodules on the thyroid gland, which are capable of secreting thyroid hormones. These nodules are not responsive to circulating TSH concentrations and so, eventually cause thyrotoxicosis. TMG is the second commonest cause of hyperthyroidism and most commonly affects older patients. Thyrotoxicosis due to a toxic multinodular goitre typically has a more insidious onset, in comparison to Graves’ disease.6 Iodine excessExcess serum iodine concentrations can also cause thyrotoxicosis. This is because thyroid hormone production is dependent upon iodine, so increased serum iodine concentrations allow increased production of the hormones. Iodine excess can occur following the use of contrast media for imaging modalities or via the contamination of food.1 IatrogenicIatrogenic causes of thyrotoxicosis include the drugs amiodarone and levothyroxine. Amiodarone contains increases iodine levels and so increases follicular thyroid hormone production. Levothyroxine is used in the management of hypothyroidism to increase thyroid hormone production where there is a deficit. Overuse of this drug can cause an inappropriately increased serum hormone concentration.1 Viral infectionViral infections can predispose to a phenomenon known as ‘subacute De Quervain’s thyroiditis’. This can cause a transient rise in thyroid hormone production due to inflammation of the thyroid gland and subsequent excessive excretion of thyroid hormones into the circulation. subacute De Quervain’s thyroiditis presents with a painful lump in the neck, most commonly between the ages of 20-50.4 Patients may subsequently develop hypothyroidism if the thyroid gland tissue is damaged by the inflammation. Postpartum thyroiditisPostpartum thyroiditis presents with a transient acute phase of thyrotoxicosis, followed by a period of hypothyroidism. This can occur 2 – 6 months following birth or miscarriage.7 Clinical featuresThyrotoxicosis presents with a wide range of clinical features due to the overall increased basal metabolic rate. HistoryTypical symptoms of thyrotoxicosis include:
Other important areas to cover in the history include:
Clinical examinationA thyroid status examination should be performed in all patients presenting with symptoms suggestive of thyrotoxicosis. Clinical features of thyrotoxicosis may include:1
Graves’ diseaseThere are some clinical features of thyrotoxicosis which are specific to Graves’ disease, due to the presence of the anti-TSHR autoantibodies. Clinical features of Graves’ disease may include:4,8
Figure 2. Thyroid eye disease Figure 3. Thyroid acropachy Figure 4. Pretibial myxoedema InvestigationsThyroid function testsThe key laboratory investigation for the diagnosis of any thyroid condition is thyroid function tests (TFTs) which include serum levels of TSH, T3 and T4. In most cases of thyrotoxicosis, the pattern of TFTs will reflect an increased production of thyroid hormones from the thyroid gland and a decreased production of pituitary TSH. This is because the HPT axis will attempt to correct the excess thyroid hormone production via negative feedback:
If thyrotoxicosis is due to a rarer pituitary cause, then there will be an increased production of pituitary TSH, causing the increased production of thyroid hormones. The pattern of TFT results will be as follows:9
See the Geeky Medics guide for a more detailed overview of thyroid function test interpretation. AutoantibodiesThe presence of thyroid autoantibodies suggests there is an underlying autoimmune disease causing thyrotoxicosis. The presence of anti-TSHR antibodies is highly suggestive of Graves’ disease.10 Other autoantibodies suggestive of autoimmune thyroid disease include anti-thyroid-peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies. These are non-specific and can be present in autoimmune causes of both hyperthyroidism (Graves’ disease) and hypothyroidism (Hashimotos’ disease).4 ImagingDoppler ultrasound may be used to image the thyroid gland, to confirm the presence of goitre and identify nodules.11 ManagementBeta-blockersBeta-blockers (commonly propranolol) are indicated in the management of thyrotoxicosis to provide symptomatic relief from the typical adrenergic symptoms (palpitations, tachycardia, tremor).4,12 Block and replaceThe block and replace management regime is commonly used for the management of hyperthyroidism in adults and is the first-line management option for hyperthyroidism in children. Block and replace involves blocking the excess thyroid hormone production from the thyroid gland and replacing this with the correct concentration of exogenous thyroid hormones. Carbimazole is used to block thyroid hormone production and levothyroxine is used to replace thyroid hormones (these medications are administered simultaneously). Patients require ongoing monitoring of their TFTs and their FBC (due to the risk of agranulocytosis associated with carbimazole). In most patients with Graves’ disease, a block and replace management regime can induce remission.12 RadioiodineRadioiodine is a definitive management option for Graves’ disease and toxic multinodular goitre. If radioiodine is deemed unsuitable for patients with Graves’ disease (e.g. due to pregnancy or malignancy), block and replace therapy is typically used as a second-line management option. If radioiodine is deemed unsuitable for patients with a toxic multinodular goitre, thyroid surgery is used as a second-line management option. Radioiodine can also be used second-line in patients with hyperthyroidism in whom block and replace has been unsuccessful.2 With radioactive iodine, measures must be taken following treatment to prevent any harm coming to those in close contact with the patient. Patients must be advised against prolonged contact with children (including their own) and pregnant women. Female patients must also be advised against becoming pregnant within the next six months following treatment and male patients must be advised against fathering children for the next four months following treatment.12 SurgeryThyroidectomy (complete removal of the thyroid gland) may be considered for the management of hyperthyroidism. Thyroidectomy is indicated in cases of thyroid malignancy, or where a thyroid goitre is causing compression of surrounding structures. Thyroidectomy may also be considered if other treatment options are unsuitable or unsuccessful.12 Removal of the thyroid gland will result in a lack of circulating thyroid hormones in these patients. Therefore, they will need to be started on long term thyroid hormone replacement, most commonly levothyroxine.4 ComplicationsThyroid stormA serious complication of thyrotoxicosis is the onset of a thyroid storm, which involves excessive adrenergic activity secondary to thyrotoxicosis. Clinical features of a thyroid storm may include:13
Thyroid storm is associated with high mortality. Cardiac complicationsCardiac complications of thyrotoxicosis include:4
Graves’ ophthalmopathyIt is important to inform patients of the complications of Graves’ ophthalmopathy. In some instances, this can also cause deterioration of visual acuity if the optic nerve is affected.14 Key points
ReviewerDr Peter KingReader in Molecular Endocrinology EditorDr Chris JefferiesReferencesText references
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