Thyroid Hormone – Anatomy, Types, Structure, Functions

Thyroid Hormone – Anatomy, Types, Structure, Functions

The thyroid hormone is well known for controlling metabolism, growth, and many other bodily functions. The thyroid gland, anterior pituitary gland, and hypothalamus comprise a self-regulatory circuit called the hypothalamic-pituitary-thyroid axis. The main hormones produced by the thyroid gland are thyroxine or tetraiodothyronine (T4) and triiodothyronine (T3). Thyrotropin-releasing hormone (TRH) from the hypothalamus, thyroid-stimulating hormone (TSH) from the anterior pituitary gland, and T4 work in synchronous harmony to maintain proper feedback mechanism and homeostasis. Hypothyroidism, caused by an underactive thyroid gland, typically manifests as bradycardia, cold intolerance, constipation, fatigue, and weight gain. In contrast, hyperthyroidism caused by increased thyroid gland function manifests as weight loss, heat intolerance, diarrhea, fine tremor, and muscle weakness.

Thyroid hormones are two hormones produced and released by the thyroid gland, namely triiodothyronine (T3) and thyroxine (T4). They are tyrosine-based hormones that are primarily responsible for the regulation of metabolism. T3 and T4 are partially composed of iodine.

Iodine is an essential trace element absorbed in the small intestine. It is an integral part of T3 and T4. Sources of iodine include iodized table salt, seafood, seaweed, and vegetables. Decreased iodine intake can cause iodine deficiency and decreased thyroid hormone synthesis. Iodine deficiency can cause cretinism, goiter, myxedema coma, and hypothyroidism.

Cellular Mechanism of Thyroid Hormone

Regulation of thyroid hormone starts at the hypothalamus. The hypothalamus releases thyrotropin-releasing hormone (TRH) into the hypothalamic-hypophyseal portal system to the anterior pituitary gland. TRH stimulates thyrotropin cells in the anterior pituitary to release of thyroid-stimulating hormone (TSH). TRH is a peptide hormone created by the cell bodies in the periventricular nucleus (PVN) of the hypothalamus. These cell bodies project their neurosecretory neurons down to the hypophyseal portal circulation, where TRH can concentrate before reaching the anterior pituitary.

TRH is a tropic hormone, meaning that it indirectly affects cells by stimulating other endocrine glands first. It binds to the TRH receptors on the anterior pituitary gland, causing a signal cascade mediated by a G-protein coupled receptor. Activation of Gq protein leads to the activation of phosphoinositide-specific phospholipase C (PLC). PLC hydrolyzes phosphatidylinositol 4,5-P(PIP) into inositol 1,4,5-triphosphate (IP) and 1,2-diacylglycerol (DAG). These second messengers mobilize intracellular calcium stores and activate protein kinase C, leading to downstream gene activation and transcription of TSH. TRH also has a non-tropic effect on the pituitary gland through the hypothalamic-pituitary-prolactin axis. As a non-tropic hormone, TRH directly stimulates lactotropic cells in the anterior pituitary to produce prolactin. Other substances like serotonin, gonadotropin-releasing hormone, and estrogen can also stimulate prolactin release. Prolactin can cause breast tissue growth and lactation.

TSH is released into the blood and binds to the thyroid-releasing hormone receptor (TSH-R) on the basolateral aspect of the thyroid follicular cell. The TSH-R is a Gs-protein coupled receptor, and its activation leads to the activation of adenylyl cyclase and intracellular levels of cAMP.  The increased cAMP activates protein kinase A (PKA). PKA phosphorylates different proteins to modify their functions. The five steps of thyroid synthesis are below:

  • Synthesis of Thyroglobulin – Thyrocytes in the thyroid follicles produce a protein called thyroglobulin (TG). TG does not contain any iodine, and it is a precursor protein stored in the lumen of follicles. It is produced in the rough endoplasmic reticulum. Golgi apparatus pack it into the vesicles, and then it enters the follicular lumen through exocytosis.
  • Iodide uptake – Protein kinase A phosphorylation causes increased activity of basolateral Na+-I- symporters, driven by Na+-K+-ATPase, to bring iodide from the circulation into the thyrocytes. Iodide then diffuses from the basolateral side to the apex of the cell, where it is transported into the colloid through the pendrin transporter.
  • Iodination of thyroglobulin – Protein kinase A also phosphorylates and activates the enzyme thyroid peroxidase (TPO). TPO has three functions: oxidation, organification, and coupling reaction.

    • Oxidation – TPO uses hydrogen peroxide to oxidize iodide (I-) to iodine (I2). NADPH-oxidase, an apical enzyme, generates hydrogen peroxide for TPO.
    • Organification – TPO links tyrosine residues of thyroglobulin protein with I2. It generates monoiodotyrosine (MIT) and diiodotyrosine (DIT). MIT has a single tyrosine residue with iodine, and DIT has two tyrosine residues with iodine.
    • Coupling reaction – TPO combines iodinated tyrosine residues to make triiodothyronine (T3) and tetraiodothyronine (T4). MIT and DIT join to form T3, and two DIT molecules form T4.
  • Storage – thyroid hormones are bound to thyroglobulin for stored in the follicular lumen.
  • Release – thyroid hormones are released into the fenestrated capillary network by thyrocytes in the following steps:

    • Thyrocytes uptake iodinated thyroglobulin via endocytosis
    • Lysosome fuse with the endosome containing iodinated thyroglobulin
    • Proteolytic enzymes in the endolysosome cleave thyroglobulin into MIT, DIT, T3, and T4.
    • T3 (20%) and T4 (80%) are released into the fenestrated capillaries via MCT8 transporter.
    • Deiodinase enzymes remove iodine molecules from DIT and MIT. Iodine can be salvaged and redistributed to an intracellular iodide pool.

Organ Systems Involved

Thyroid hormone affects virtually every organ system in the body, including the heart, CNS, autonomic nervous system, bone, GI, and metabolism. In general, when the thyroid hormone binds to its intranuclear receptor, it activates the genes for increasing metabolic rate and thermogenesis. Increasing metabolic rate involves increased oxygen and energy consumption.

  • Heart – thyroid hormones have a permissive effect on catecholamines. It increases the expression of beta-receptors to increase heart rate, stroke volume, cardiac output, and contractility.
  • Lungs – thyroid hormones stimulate the respiratory centers and lead to increased oxygenation because of increased perfusion.
  • Skeletal muscles – thyroid hormones cause increased development of type II muscle fibers. These are fast-twitch muscle fibers capable of fast and powerful contractions.
  • Metabolism – thyroid hormone increases the basal metabolic rate. It increases the gene expression of Na+/K+ ATPase in different tissues leading to increased oxygen consumption, respiration rate, and body temperature. Depending on the metabolic status, it can induce lipolysis or lipid synthesis. Thyroid hormones stimulate the metabolism of carbohydrates and anabolism of proteins. Thyroid hormones can also induce the catabolism of proteins in high doses. Thyroid hormones do not change the blood glucose level, but they can cause increased glucose reabsorption, gluconeogenesis, glycogen synthesis, and glucose oxidation.
  • Growth during childhood – In children, thyroid hormones act synergistically with growth hormones to stimulate bone growth. It induces chondrocytes, osteoblasts, and osteoclasts. Thyroid hormone also helps with brain maturation by axonal growth and the formation of the myelin sheath.
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Synthesis of the thyroid hormones, as seen on an individual thyroid follicular cell[rx]

  • Thyroglobulin is synthesized in the rough endoplasmic reticulum and follows the secretory pathway to enter the colloid in the lumen of the thyroid follicle by exocytosis.
  • Meanwhile, a sodium-iodide (Na/I) symporter pumps iodide (I) actively into the cell, which previously has crossed the endothelium by largely unknown mechanisms.
  •  This iodide enters the follicular lumen from the cytoplasm by the transporter pendrin, in a purportedly passive manner.
  • In the colloid, iodide (I) is oxidized to iodine (I) by an enzyme called thyroid peroxidase.
  • Iodine (I) is very reactive and iodinates the thyroglobulin at tyrosyl residues in its protein chain (in total containing approximately 120 tyrosyl residues).
  • In conjugation, adjacent tyrosyl residues are paired together.
  • Thyroglobulin re-enters the follicular cell by endocytosis.
  • Proteolysis by various proteases liberates thyroxine and triiodothyronine molecules
  • Efflux of thyroxine and triiodothyronine from follicular cells, which appears to be largely through monocarboxylate transporter (MCT) 8 and 10,[rx][rx] and entry into the blood.

Thyroid hormones (T4 and T3) are produced by the follicular cells of the thyroid gland and are regulated by TSH made by the thyrotropes of the anterior pituitary gland. The effects of T4 in vivo are mediated via T3 (T4 is converted to T3 in target tissues). T3 is three to five times as active as T4.

Thyroxine (3,5,3′,5′-tetraiodothyronine) is produced by follicular cells of the thyroid gland. It is produced as the precursor thyroglobulin (this is not the same as thyroxine-binding globulin (TBG)), which is cleaved by enzymes to produce active T4.

The steps in this process are as follows:[rx]

  • The Na+/I symporter transports two sodium ions across the basement membrane of the follicular cells along with an iodide ion. This is a secondary active transporter that utilizes the concentration gradient of Na+ to move I against its concentration gradient.
  • I is moved across the apical membrane into the colloid of the follicle by pendrin.
  • Thyroperoxidase oxidizes two I to form I2. Iodide is non-reactive, and only the more reactive iodine is required for the next step.
  • The thyroperoxidase iodinates the tyrosyl residues of the thyroglobulin within the colloid. The thyroglobulin was synthesized in the ER of the follicular cell and secreted into the colloid.
  • Iodinated Thyroglobulin binds megalin for endocytosis back into cell.
  • Thyroid-stimulating hormone (TSH) released from the anterior pituitary (also known as the adenohypophysis) binds the TSH receptor (a Gs protein-coupled receptor) on the basolateral membrane of the cell and stimulates the endocytosis of the colloid.
  • The endocytosed vesicles fuse with the lysosomes of the follicular cell. The lysosomal enzymes cleave the T4 from the iodinated thyroglobulin.
  • The thyroid hormones cross the follicular cell membrane towards the blood vessels by an unknown mechanism.[rx] Textbooks have stated that diffusion is the main means of transport,[rx] but recent studies indicate that monocarboxylate transporter (MCT) 8 and 10 play major roles in the efflux of the thyroid hormones from the thyroid cells.[rx][rx]

The Function of Thyroid Hormone

  • Metabolic – The thyroid hormones increase the basal metabolic rate and have effects on almost all body tissues.[rx] Appetite, the absorption of substances, and gut motility are all influenced by thyroid hormones.[rx] They increase the absorption in the gut, generation, uptake by cells, and breakdown of glucose.[rx] They stimulate the breakdown of fats, and increase the number of free fatty acids.[rx] Despite increasing free fatty acids, thyroid hormones decrease cholesterol levels, perhaps by increasing the rate of secretion of cholesterol in bile.[rx]
  • Cardiovascular – The hormones increase the rate and strength of the heartbeat. They increase the rate of breathing, intake and consumption of oxygen, and increase the activity of mitochondria.[rx] Combined, these factors increase blood flow and the body’s temperature.[rx]
  • Developmental – Thyroid hormones are important for normal development.[rx] They increase the growth rate of young people,[rx] and cells of the developing brain are a major target for the thyroid hormones T3 and T4. Thyroid hormones play a particularly crucial role in brain maturation during fetal development and the first few years of postnatal life[rx]
  • The thyroid hormones also play a role in maintaining normal sexual function, sleep, and thought patterns. Increased levels are associated with increased speed of thought generation but decreased focus.[rx] Sexual function, including libido and the maintenance of a normal menstrual cycle, is influenced by thyroid hormones.[rx]

Some of the essential functions of the thyroid hormones are as follows

  • They help in the overall growth, development, and differentiation of all the cells of the body.
  • They regulate the basal metabolic rate (BMR).
  • They play an important role in calcium metabolism
  • They help in the overall development and function of CNS in children.
  • They stimulate somatic and psychic growth.
  • They stimulate heart rate and contraction.
  • They help in the deposition of calcium and phosphate in bone and make the bones strong.
  • They decrease the level of calcium in the blood.
  • They regulate carbohydrate, fat, and protein metabolism.
  • They also help in the metabolism of vitamins.
  • They regulate the body temperature.
  • They help degrade cholesterol and triglycerides.
  • They maintain the electrolyte balance.
  • They support the process of RBC formation.
  • They enhance mitochondrial metabolism.
  • They increase the oxygen consumptions of the cells and tissues.
  • They influence the mood and behavior of a person.
  • They stimulate gut motility.
  • They also enhance the sensitivity of the beta-adrenergic receptors to catecholamines.

The physiological effects of thyroid hormones are listed below

  • Increases the basal metabolic rate
  • Depending on the metabolic status, it can induce lipolysis or lipid synthesis.
  • Stimulate the metabolism of carbohydrates
  • Anabolism of proteins. Thyroid hormones can also induce the catabolism of proteins in high doses.
  • Permissive effect on catecholamines
  • In children, thyroid hormones act synergistically with growth hormones to stimulate bone growth.
  • The impact of thyroid hormone in CNS is important. During the prenatal period, it is needed for the maturation of the brain. In adults, it can affect mood. Hyperthyroidism can lead to hyperexcitability and irritability. Hypothyroidism can cause impaired memory, slowed speech, and sleepiness.
  • Thyroid hormone affects fertility, ovulation, and menstruation.


Thyroid hormones are lipophilic and circulate bound to the transport proteins. Only a fraction (approximately 0.2%) of the thyroid hormone (free T4) is unbound and active. Transporter proteins include thyroxine-binding globulin (TBG), transthyretin, and albumin. TBG transports the majority (two-thirds) of the T4, and transthyretin transports thyroxine and retinol. When it reaches its target site, T3 and T4 can dissociate from their binding protein to enter cells either by diffusion or carrier-mediated transport. Receptors for T3 bind are already bound to the DNA in the nucleus before the ligand binding. T3 or T4 then bind to nuclear alpha or beta receptors in the respective tissue and cause activation of transcription factors leading to the activation of certain genes and cell-specific responses. Thyroid hormones are degraded in the liver via sulfation and glucuronidation and excreted in the bile.

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Thyroid receptors are transcription factors that can bind to both T3 and T4. However, they have a much higher affinity for T3. As a result, T4 is relatively inactive. Deiodinases convert T4 to active T3 or inactive reverse T3 (rT3). There are three types of deiodinases: type I, II, and III. Type I (DIO1) and II (DIO2) are located in the liver, kidneys, muscles, and thyroid glands. Type III (DIO3) deiodinases are located in the CNS and placenta. DIO1 and DIO2 convert T4 to the active form T3, and DIO3 converts T4 into inactive form rT3.

Clinical Significance

  • Goiter – It is a condition where the thyroid gland shows an abnormal enlargement. Goiters broadly classify into uni-nodular, multinodular, and diffuse types. Each further includes many different types of goiters. Some of the commonest with some of their important features are described below.
  • Colloid nodular goiter – This is the commonest of the non-neoplastic lesions of the thyroid. In these types of goiter, the thyroid follicles are filled with an abundant amount of colloid in their lumens and lined by squamous follicular cells.
  • Hyperthyroidism (Thyrotoxicosis) – It is a condition of hypermetabolic state and hyperfunctioning of the thyroid gland resulting in increased T3 and T4 levels. Some symptoms included palpitations, tachycardia, nervousness, etc.
  • Graves disease – This disease is a combination of thyrotoxicosis, exophthalmos, and dermopathy (myxedema). It is especially seen in women in the age group of 20 to 40 years, manifesting in the form of prolonged and violent palpitations.
  • Thyroid cancer – Thyroid carcinomas arise either from the follicular epithelium or parafollicular C-cells. They are painless nodules and compression, displaces the adjacent structures. The carcinomas of the thyroid can manifest in the form of papillary carcinoma, follicular carcinoma, anaplastic carcinoma, and medullary carcinoma.
  • Thyroiditis – Inflammation of the thyroid, usually from a viral infection or autoimmune condition. Thyroiditis can be painful or have no symptoms at all.
  • Thyroid cancer – An uncommon form of cancer, thyroid cancer is usually curable. Surgery, radiation, and hormone treatments may be used to treat thyroid cancer.
  • Thyroid nodule – A small abnormal mass or lump in the thyroid gland. Thyroid nodules are extremely common. Few are cancerous. They may secrete excess hormones, causing hyperthyroidism, or cause no problems.
  • Thyroid storm – A rare form of hyperthyroidism in which extremely high thyroid hormone levels cause severe illness.

Symptoms of Hypothyroidism

Generalized decreased basal metabolic rate can present as apathy, slowed cognition, skin dryness, alopecia, increased low-density lipoproteins, and increased triglycerides. Hypothyroidism must be ruled out in psychiatry patients presenting with apathy and slowed cognition. Hypothyroidism can decrease sympathetic activity leading to decreased sweating, bradycardia, and constipation. Patients can present with myopathy and decreased cardiac output because of decreased transcription of sarcolemmal genes.

Hyperprolactinemia can be caused by hypothyroidism. Thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates prolactin and TSH release. Prolactin release can suppress testosterone, LH, FSH, and GnRH release. Prolactin can also cause breast tissue growth.

Patients with hypothyroidism may present with myxedema caused by decreased clearance of complex glycosaminoglycans and hyaluronic acids from the reticular layer of the dermis. Initially, the nonpitting edema is pretibial. As the state of hypothyroidism continues, patients can develop generalized edema.

Symptoms related to decreased metabolic rate

  • Bradycardia
  • Fatigue
  • Cold intolerance
  • Weight gain
  • Poor appetite
  • Hair loss
  • Cold and dry skin
  • Constipation
  • Myopathy, stiffness, cramps, entrapment syndromes
  • Delayed deep tendon reflex relaxation

Symptoms from generalized myxedema

  • Myxedematous heart disease
  • Puffy appearance with doughy skin texture
  • Hoarse voice with difficulty articulate words
  • Pretibial and periorbital edema

Symptoms of hyperprolactinemia

  • Amenorrhea or menorrhagia
  • Galactorrhea
  • Erectile dysfunction, infertility in men
  • Decreased libido

Other symptoms

  • Depression
  • Impaired concentration and memory
  • Goiter
  • Hypertension

Congenital hypothyroidism

  • Umbilical hernia
  • Hypotonia
  • Prolonged neonatal jaundice
  • Poor feeding, absence of thirst (adipsia)
  • Decreased activity
  • Pot-belly, puffy-face, protuberant tongue
  • Poor brain development

Symptoms of Hyperthyroidism

Generalized hypermetabolism from hyperthyroidism causes increased Na+/K+-ATPase to promote thermogenesis. There is increased catecholamine secretion and, beta-adrenergic receptors are also upregulated in various tissues. As a result of the hyperadrenergic state, peripheral vascular resistance is decreased. In the heart, hyperthyroidism causes a decreased amount of phospholamban, a protein that normally decreases the affinity of calcium-ATPase for calcium in the sarcoplasmic reticulum. As a result of decreased phospholamban, there is increased Ca+ movement between the sarcoplasmic reticulum and cytosol, leading to increased contractility. Increased beta-receptors on the heart also lead to increased cardiac output.


  • Heat intolerance
  • Weight loss
  • Increased appetite
  • Increased sweating from cutaneous blood flow increase
  • Weakness
  • Fatigue
  • Onycholysis (separation of nails from nail beds)
  • Pretibial myxedema


  • Lid lag (when looking down, sclera visible above cornea)
  • Lid retraction (when looking straight, sclera visible above the cornea)
  • Graves ophthalmopathy


  • Diffuse, smooth, non-tender goiter
  • The audible bruit can be heard at the superior poles


  • Tachycardia (can be masked by patients taking beta-blockers)
  • Palpitations
  • An irregular pulse from atrial fibrillation
  • Hypertension
  • Widened pulse pressure because systolic pressure increases and diastolic pressure decreases
  • Heart failure (elderly patients)
  • Chest pain
  • Abnormal heart rhythms


  • Fine tremors of the outstretched fingers. Face, tongue, and head can also be involved. Tremors respond well to treatment with beta-blockers.
  • Myopathy affecting proximal muscles. Serum creatine kinase levels can be normal.
  • Osteoporosis, caused by the direct effects of T3. Elderly patients can present with fractures.

Neuropsychiatric system

  • Restlessness
  • Anxiety
  • Depression
  • Emotional instability
  • Insomnia
  • Tremoulousness
  • Hyperreflexia

Conditions associated with hypothyroidism

  • Iodine deficiency 
  • Cretinism 
  • Wolff-Chaikoff effect
  • Subacute thyroiditis 
  • Postpartum thyroiditis 
  • Riedel thyroiditis 
  • Hashimoto thyroiditis 
  • Drug-induced 

Conditions associated with hyperthyroidism

  • Graves disease 
  • Iodine excess 
  • Struma ovarii 
  • Thyrotropic pituitary adenoma 
  • Jod-Basedow phenomenon 
  • Drug-induced: amiodarone, lithium 
  • Thyrotoxicosis and thyroid storm 
  • Toxic multinodular goiter 
  • Thyroid adenoma 


History and Physical

Subclinical hypothyroidism is asymptomatic most of the time. However, it can present with symptoms of hypothyroidism. It is essential to assess hypothyroid symptoms as it influences whether thyroid replacement therapy requires initiation. The clinical features of hypothyroidism are as follows:

  • Integumentary: Dry skin, hair loss, loss of outer 1/3rd of eyebrows, facial puffiness.
  • Gastrointestinal: Constipation, dysphagia, loss of appetite, weight gain, cholelithiasis
  • Cardiovascular: Diastolic hypertension, bradycardia, pericardial effusions.
  • Neurological: Decreased attention span, pseudodementia, mononeuropathies (most commonly carpal tunnel syndrome)
  • Musculoskeletal: Muscular weakness, cramps, stiffness, fatigue.
  • Reproductive: Irregular periods, decreased libido.

Hypothalamus releases thyrotropin-releasing hormone (TRH) that stimulates the secretion of TSH in the pituitary gland. Increased free T4 and T3 inhibit the release of TRH and TSH through a negative feedback loop. As a result, T3 and T4 secretion and iodine uptake are reduced. Other hormones, such as somatostatin, glucocorticoids, and dopamine, also inhibit TSH production. Cold, stress, and exercise increase TRH release.

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The initial tests of choice to screen for any thyroid abnormality are a TSH and free thyroxine (free T4) test. These determine whether the abnormality arises centrally from the thyroid gland (primary), peripherally from the pituitary (secondary), or hypothalamus (tertiary). In primary hypothyroidism is suspected, the thyroid gland is not releasing enough thyroid hormones. Therefore, TSH levels will be appropriately elevated, while free T4 levels will be lower. In primary hyperthyroidism, free T4 levels abnormally increased, and TSH levels will be appropriately decreased. Other lab tests such as TSH receptor antibodies or antibodies to thyroid peroxidase can help aid in diagnosing Graves disease or Hashimoto thyroiditis, respectively.

In pregnant women, thyroid-binding globulin production is increased because of estrogen and beta-human chorionic gonadotropin (beta-HCG). More free T4 will be bound to TGB, leading to increased production of T4. TSH levels and free T4 levels will normalize, and total T4 will increase. Therefore, laboratory values will show normal TSH, normal free T4, and elevated total T4.

Thyroid Tests

  • Anti-TPO antibodies – In autoimmune thyroid disease, proteins mistakenly attack the thyroid peroxidase enzyme, which is used by the thyroid to make thyroid hormones.
  • Thyroid ultrasound – A probe is placed on the skin of the neck, and reflected sound waves can detect abnormal areas of thyroid tissue.
  • Thyroid scan – A small amount of radioactive iodine is given by mouth to get images of the thyroid gland. Radioactive iodine is concentrated within the thyroid gland.
  • Thyroid biopsy – A small amount of thyroid tissue is removed, usually to look for thyroid cancer. A thyroid biopsy is typically done with a needle.
  • Thyroid-stimulating hormone (TSH) – Secreted by the brain, TSH regulates thyroid hormone release. A blood test with high TSH indicates low levels of thyroid hormone (hypothyroidism), and low TSH suggests hyperthyroidism.
  • T3 and T4 (thyroxine) – The primary forms of thyroid hormone, checked with a blood test.
  • Thyroglobulins – A substance secreted by the thyroid that can be used as a marker of thyroid cancer. It is often measured during follow-up in patients with thyroid cancer. High levels indicate recurrence of cancer.
  • Other imaging tests – If thyroid cancer has spread (metastasized), tests such as CT scans, MRI scans, or PET scans can help identify the extent of spread.

Thyroid Treatments

Antithyroid drugs that work in the thyroid gland 

  • Perchlorate – inhibits Na+/I- symporter – blocks iodide uptake
  • Thionamides – inhibits TPO – block thyroid hormone synthesis
  • Iodide > 5mg – inhibits Na+/I- symporter and TPO – blocks iodide uptake and thyroid hormone synthesis
  • Lithium – inhibits thyroid hormone release (off-label use for thyroid storm)
  • Thyroid surgery (thyroidectomy) – A surgeon removes all or part of the thyroid in an operation. Thyroidectomy is performed for thyroid cancer, goiter,  or hyperthyroidism.
  • Antithyroid medications – Drugs can slow down the overproduction of thyroid hormone in hyperthyroidism. Two common antithyroid medicines are methimazole and propylthiouracil.
  • Radioactive iodine – Iodine with radioactivity that can be used in low doses to test the thyroid gland or destroy an overactive gland. Large doses can be used to destroy cancerous tissue.
  • External radiation – A beam of radiation is directed at the thyroid, on multiple appointments. The high-energy rays help kill thyroid cancer cells.
  • Thyroid hormone pills – Daily treatment that replaces the amount of thyroid hormone you can no longer make. Thyroid hormone pills treat hypothyroidism and are also used to help prevent thyroid cancer from coming back after treatment.
  • Recombinant human TSH – Injecting this thyroid-stimulating agent can make thyroid cancer show up more clearly on imaging tests.

Antithyroid drugs that work in peripheral tissue – all these drugs inhibit the deiodinase enzymes. Deiodinase enzymes normally convert T4 into the active form T3. These drugs inhibit the conversion of T4 to T3 and reduce its activity.

  • Propylthiouracil (thionamide)
  • Dexamethasone
  • Amiodarone
  • Propranolol


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