- Triiodothyronine | You and Your Hormones from the Society for Endocrinology
- How is triiodothyronine controlled?
- What happens if I have too much triiodothyronine?
- What happens if I have too little triiodothyronine?
- Thyroid Hormones (T3, T4): Roles, Functions, High/Low Levels
- What are T3 and T4?
- Thyroid Hormones Roles and Functions
- Mitochondrial Function
- Circadian Rhythm
- Cognitive Function
- Anticancer Effects
- Heart Health
- Bone Health
- Thyroid Blood Tests & Panels
- Physiology, Thyroid Stimulating Hormone (TSH)
- Understanding thyroid tests
- Thyroxine (T4) Test: MedlinePlus Lab Test Information
Triiodothyronine | You and Your Hormones from the Society for Endocrinology
Triiodothyronine is the active form of the thyroid hormone, thyroxine. Approximately 20% of triiodothyronine is secreted into the bloodstream directly by the thyroid gland.
The remaining 80% is produced from conversion of thyroxine by organs such as the liver and kidneys.
Thyroid hormones play vital roles in regulating the body’s metabolic rate, heart and digestive functions, muscle control, brain development and function, and the maintenance of bones.
How is triiodothyronine controlled?
The production and release of thyroid hormones, thyroxine and triiodothyronine, is controlled by a feedback loop involving the hypothalamus, pituitary gland and thyroid gland.
Activation of thyroid hormones is then controlled in body tissues such as the liver, brain and kidneys by enzymes called deiodinases which convert thyroxine into the active form triiodothyronine.
Most of the body’s circulating triiodothyronine (about 80%) is produced in this way.
The thyroid hormone production system is regulated by a feedback loop so that when the levels of the thyroid hormones thyroxine and triiodothyronine increase, they prevent the release of both thyrotropin-releasing hormone from the hypothalamus and thyroid stimulating hormone from the pituitary gland. This system allows the body to maintain a constant level of thyroid hormones in the body.
What happens if I have too much triiodothyronine?
Thyrotoxicosis is the name of the condition in which people have too much thyroid hormone in their bloodstreams. It may result from overactivity of the thyroid gland (hyperthyroidism) from conditions such as Graves' disease, inflammation of the thyroid or a benign tumour.
Thyrotoxicosis may be recognised by a goitre, which is a swelling of the neck due to enlargement of the thyroid.
Other symptoms of thyrotoxicosis include heat intolerance, weight loss, increased appetite, increased bowel movements, irregular menstrual cycle, rapid or irregular heartbeat, palpitations, tiredness, irritability, tremor, hair thinning/loss and retraction of the eyelids, which results in a ‘staring’ appearance.
What happens if I have too little triiodothyronine?
Hypothyroidism is the term for the production of too little thyroid hormone by the thyroid gland.
This may be because of autoimmune diseases (such as Hashimoto’s disease), very poor iodine intake or due to some medications.
Since thyroid hormones are essential for physical and mental development, untreated hypothyroidism before birth and during childhood can result in learning disability and reduced growth.
Hypothyroidism in adults results in a slowing of the body’s functions with symptoms such as tiredness, intolerance to cold temperatures, low heart rate, weight gain, reduced appetite, poor memory, depression, stiffness of the muscles and reduced fertility. See the article on hypothyroidism for more information.
Last reviewed: Mar 2018
Thyroid Hormones (T3, T4): Roles, Functions, High/Low Levels
The thyroid hormones (T3 & T4) stimulate energy metabolism, regulate immunity, support cognitive development, and more. Due to their complex metabolic roles, it’s essential for overall health to keep them in the normal range. Read on to learn the diverse functions of thyroid hormones, blood test reference values, and the consequences of high/low levels.
What are T3 and T4?
The thyroid gland is located in the base of your neck and is involved in secreting important hormones T4 (thyroxine) and T3 (triiodothyronine).
T3 contains 3 iodine atoms and is created from the breakdown of T4. The breakdown of T4 is encouraged by the thyroid-stimulating hormone.
T4 is synthesized from residues of the amino acid tyrosine, found in thyroglobulin (a protein created in the thyroid). It contains 4 iodine atoms and allows the body to better control the more active T3.
If there are not enough thyroid hormones in the bloodstream, the hypothalamus will signal the pituitary gland (via TRH) to produce TSH for the thyroid to release more T3 and T4.
Reverse T3 (rT3) is the mirror image of T3. It competes with T3 and binds to the thyroid receptor but does not activate it.
Thyroid Hormones Roles and Functions
T3 and T4 affect :
- Heart rate
- The nervous system
- Muscle strength
- Menstrual cycles
- Body temperature
- Cholesterol levels
- Growth and development
- Intestinal flow
T3 changes gene expression (cellular production of certain proteins and hormones) of multiple metabolism-related genes.
These genes include PPAR-gamma, NRF1, NRF2, and other transcription factors that work with them .
Thyroid hormone may work in synergy with other receptors, including RXR (vitamin A receptor), or VDR (vitamin D receptor) .
T3 stimulates oxygen consumption and heat production by the mitochondria, and the production of new mitochondria [4, 5].
Therefore, mitochondrial dysfunction can result in symptoms of hypothyroidism, even in the presence of healthy levels of thyroid hormones.
Immune cells have receptors for T3, and the administration of T3 increases the size and growth of cells in the thymus .
In mice, T4 treatment suppresses antibody synthesis and growth of white blood cells .
Both T4 and T3 enhance interferon-induced (stimulated) natural killer cells but don’t impact the baseline natural killer cell activity .
TNF-alpha and interferons induce production of class I and II HLA antigens in human thyroid cells (thyrocytes), which cause autoimmunity, as patients with autoimmune thyroid disorders have increased HLA class I and II antigens. The thyroid cells themselves produce IL-1 and IL-6 .
The immune system is weakened with stress, making the body more receptive of autoimmune (a condition where the immune system attacks itself) thyroid conditions (eg, Hashimoto’s thyroiditis) .
A study found that newly-born rats used their thyroid hormones to regulate the number of neural mast cells, which release histamine as an inflammatory immune response .
Histamine decreases T3 and T4 for a short amount of time (15 to 30 minutes) .
TSH is lower during the daytime and increases at night around the time we go to sleep. Our biological clock (suprachiasmatic nucleus or SCN) communicates with cells that produce TRH in the hypothalamus. However, T3 and T4 fluctuate much less than TSH, perhaps because they take much longer to produce and degrade in the blood .
In depressed people, the nighttime TSH surge doesn’t happen. In addition, this fluctuation of TSH is abnormal in certain other diseases .
In healthy men, leptin and TSH fluctuate similarly over 24 hours. The fluctuation of TSH was not observed in men who are deficient in leptin .
Nerve cells that control the TRH production and release have receptors for a-MSH .
Thyroid hormones are essential for cognitive development and functions. People with sufficient levels generally perform better on cognitive tasks and process information more efficiently. The lack of thyroid hormones can result in a range of cognitive disorders, from mild impairments to severe developmental disorders .
Thyroid hormones regulate nervous system-related growth. In particular, the central nervous system (which consists of the brain and spinal cord) needs T3 and T4 to upkeep normal development. A drug, L-T4 (which consists of T4), when administered to rats, enhanced spatial memory .
While fixing thyroid problems may help normalize mood and cognitive ability, a severe hypothyroidism cognitive failure will not be completely cured .
Subclinical hyperthyroidism (an elevated level of TH with a decreased level of TSH) and higher free T4 within the normal range may cause decreases in thinking ability [18, 19].
Increased total T3 count was related to lower overall cognitive ability in people with mild cognitive impairment. Those with higher than average total T3 counts had trouble with remembering, visuospatial skills, planning, and emotional regulation .
studies in rats, T3 along with electroconvulsive shock therapy may be a viable alternative to lithium with electroconvulsive shock therapy because the lithium treatment has shown cognitive damage in patients .
Thyroid hormone receptors may be useful as tumor suppressors [22, 23, 24].
Incorrectly formed thyroid hormone receptors might lead to acute erythroleukemia (immature red and white blood cells crowd out the body) and sarcomas (connective or nonepithelial tissue cancers). Defects in the production of thyroid hormone receptors may correlate with a higher prevalence of breast, lung, and thyroid cancers .
T3 can make heart contractions harder and dilate the blood vessels .
Overt hyperthyroidism induces a state of a faster heart rate, especially atrial fibrillation (irregularly quick heart rate that causes poor circulation), whereas overt hypothyroidism is characterized by the opposite changes.
Subclinical hypothyroidism causes heart rate problems and an enhanced risk for atherosclerosis and myocardial infarction (heart attack). L-thyroxine (L-T4) or 3,5-diiodothyropropionic acid administered in a timely manner help prevent heart complications [26, 27, 28].
Thyroid hormones increase oxygen consumption and glucose uptake because oxygen and glucose are used in providing energy for the body .
In rats, lower thyroid hormones correlated with lower levels of insulin (a storage hormone for glucose) [30, 31].
Thyroid hormones encourage protein breakdown and glucose exchange throughout cells and insulin .
Thyroid dysfunction often goes hand in hand with insulin resistance .
T3 improved insulin production and blood glucose control in mice .
Hypothyroidism in children leads to delayed growth, while thyrotoxicosis makes bones mature so quickly that children’s bones fuse before the child is ready. T3 builds up bone mass but also can break down bones in adults to increase new bone growth [35, 36, 37].
T4 and T3 supplements can be used for hypothyroid children with inadequate bone development .
Thyroid Blood Tests & Panels
|Measurement||Full Name||Unit||Reference Range|
|fT3||Free T3||pg/ml||2.5 – 4.3|
|fT4||Free T4||ng/dL||0.9 – 1.7|
|T3||Triiodothyronine (free and bound)||ng/dL||75 – 200|
|T4||Tetraiodothyronine or Thyroxine (free T4)||ug/dL||6 – 12|
|TBG||Thyroxine Binding Globulin||mg/dL||1.1 – 2.1|
Physiology, Thyroid Stimulating Hormone (TSH)
Thyroid-stimulating hormone (TSH) is crucial for the modulation of thyroid hormone release and growth of the thyroid gland. The hypothalamic-pituitary axis regulates TSH release.
The hypothalamus releases thyroid-releasing hormone (TRH), which stimulates thyrotrophs of the anterior pituitary to secrete TSH.
TSH is released by the anterior pituitary and stimulates the thyroid follicular cells to release thyroxine, T4 (80%) and triiodothyronine, or T3 (20%). When T4 is released into circulation, it can be converted to T3 through the process of de-iodination.
T4 and T3 can then exert negative feedback on TSH levels with high levels of T3/T4 decreasing TSH and low levels of T3/T4 increasing TSH levels from the anterior pituitary. In this review, we discuss the physiology, biochemistry, and clinical relevance of TSH .
TSH is the accepted first-line screening test for the diagnosis of the majority of patients suspected of having hypothyroidism or hyperthyroidism and is measured by automated immunoassays.
In primary disease, the disease originates in the thyroid gland itself.
If the thyroid gland is secreting high levels of T3/T4, this will negatively feedback on the anterior pituitary and thus, decrease the secretion of TSH.
If the thyroid gland is secreting low levels of T3/T4, the absence of negative feedback on the anterior pituitary will increase TSH secretion from the anterior pituitary.
For secondary disease or central hyperthyroid or hypothyroid disease, the disease originates in the anterior pituitary itself.
If a tumor in the anterior pituitary is secreting excessively high TSH, this will stimulate the thyroid follicular cells to secrete high levels of T3/T4.
If the anterior pituitary is secreting low levels of TSH such as in panhypopituitarism, this lack of stimulation of thyroid follicular cells will cause them to secrete low levels of T4.
To assess whether thyroid disease is primary or secondary, the TSH must be evaluated in comparison to T3/T4 levels. If TSH and T3/T4 both increase or both decrease together, this indicates either secondary (central) hypothyroidism or secondary hyperthyroidism. However, if the TSH and T3/T4 change in the opposite directions, this indicates primary thyroid disease.
TSH is a peptide hormone produced by the anterior pituitary. Specifically, it is composed of 2 chains: 1 alpha, and 1 beta chain and has a molecular mass of approximately 28,000 Da.
This also holds true for other glycoprotein hormones made by the anterior pituitary, including luteinizing hormone (LH), follicle-stimulating hormone (FSH), and human chorionic gonadotropin (HCG). This is important because TSH has the same alpha subunit as LH, FSH, and HCG. However, TSH has a different beta chain than LH, FSH, and HCG that confers biological specificity.
Since TSH, LH, FSH, and HCG all have the alpha subunit, they all have the cyclic adenine monophosphate (cAMP) second messenger system. TSH also activates the IP3 signaling cascade. The cAMP second messenger system entails adenine monophosphate (AMP) conversion to cAMP, and the IP3 second messenger system involves calcium release from the sarcoplasmic reticulum.
The cAMP and IP3/Ca2+ then leads to downstream physiological effects. There is a diurnal variation in TSH secretion with highest values between midnight and 4:00 am and lowest values in the late afternoon.
Thyroid hormone receptor subtypes are expressed in different tissues. The thyroid hormone receptor alpha (TRa) is predominantly expressed in the brain, heart, and bone.
The thyroid hormone receptor beta (TRb1) is expressed in the liver, kidney, and thyroid. The TRb2 is primarily in the retina, cochlea, and pituitary.
Mutations in TRa or TRb can result in disease which is beyond the scope of this review.
TSH modulates the release of T3/T4 from thyroid follicular cells. T4 is deiodinated to T3, which is a more potent thyroid hormone. While about 20% of T3 originates from the thyroid gland, 80% of T3 is produced by peripheral conversion via a deiodinase.
More than 99% of thyroid hormone is protein bound to thyroid binding globulin, prealbumin, and albumin.
T3 then binds to its receptor in the nucleus; this activates the transcription of DNA, which promotes translation of mRNA, which activates the synthesis of new proteins.
These new proteins influence many organ systems, promoting growth and bone maturation as well as maturation of the central nervous system (CNS). The basal metabolic rate is increased, with an increase in synthesis of Na+-K+ ATPases, increase in oxygen consumption, and increased heat production.
Metabolism is activated as well, with an increase in glucose absorption, glycogenolysis, gluconeogenesis, lipolysis, and protein synthesis and degradation (net catabolic).
These proteins also influence the cardiovascular system by increasing cardiac output by increasing the number of beta-1 receptors on the myocardium such that the myocardium is more sensitive to stimulation by the sympathetic nervous system, thereby increasing contractility.
The hypothalamic-pituitary axis regulates TSH release. The hypothalamus secretes the thyroid releasing hormone (TRH), which stimulates thyrotrophs in the anterior pituitary to secrete TSH.
TSH is released by the anterior pituitary and stimulates the thyroid follicular cells to release thyroxine, or T4 (80%) and triiodothyronine, or T3 (20%). When T4 is released into circulation, it can be converted to T3 through the process of deiodination.
T4 and T3 can then exert negative feedback on TSH levels, with high levels of T3/T4 decreasing TSH and low levels of T3/T4 increasing TSH levels from the anterior pituitary. T3 is the predominant inhibitor of TSH secretion.
Because TSH secretion is so sensitive to minor changes in serum-free T4 through this negative feedback loop, abnormal TSH levels are detected earlier than those of free T4 in hypothyroidism and hyperthyroidism. There is a log-linear relationship between T3/T4 and TSH with minor changes in TH results in major changes in TSH.
TSH binds and activates the TSH receptor (TSHR), which is a G-protein coupled receptor (GPCR) on the basolateral surface of thyroid follicle cells. TSHR is coupled to both Gs and Gq G-proteins, activating both the cAMP pathway (via Gsa) and the phosphoinositol/calcium (IP/Ca2+; via Gq) second messenger signaling cascades.
The Gs pathway activates iodide uptake, thyroid hormone secretion, and gland growth and differentiation. The Gq pathway is rate-limiting for hormone synthesis by stimulating iodide organification.
A gain in function mutation of the TSH receptor can result in hyperthyroidism, while the loss in function mutations can result in hypothyroidism.
Testing for TSH is a first-line screening test for both hypothyroidism and hyperthyroidism. If values are outside the reference range of 0.4 to 4.5 uIU/ml, one reflex to measuring T4 if TSH is elevated, or T4 and T3 if TSH is decreased.
However, TSH is the best first test in both the evaluation of hypothyroidism and hyperthyroidism as the test is more reliable than plasma T3/T4 which fluctuates. In hypothyroidism, if the cause is primary (originating in the thyroid gland itself), high TSH would be detected, and this is the best first-line test.
This would be accompanied by low total T4, low free T4, hypercholesterolemia (decreased LDL receptor synthesis), and elevated creatinine kinase levels and thyroid antibodies in Hashimoto disease.
In hyperthyroidism, if the cause is primarily originating in the thyroid gland itself, for example, in patients with Graves disease with low TSH, this is the best first test. This would be accompanied by high total T4, high free T4, and elevated T3 levels. T3 levels increase before T4 levels in hyperthyroidism.
However, when TSH is elevated for reasons other than subclinical (normal T4 and T3) and clinical hypothyroidism, one needs to consider a TSH-producing tumor.
This is especially true if T4 and T3 are elevated, and the patient has features of hyperthyroidism including a goiter or selective pituitary thyroid hormone resistance syndrome due to a defect in the beta subunit of the thyroid hormone receptor. With a TSH tumor, there is an increase in alpha subunit/TSH molar ratio and the MRI scan can reveal a tumor.
Also, interference by heterophile antibodies can result in a spurious isolated increase in TSH levels since TSH is now measured by third generation sensitive immunometric “sandwich” assays with a capture and detection antibodies. The most typical heterophile antibody that interferes with the TSH assay is a human anti-mouse antibody.
When TSH levels are low, the primary diagnosis is hyperthyroidism. However, patients treated with thyroxine can have low levels, for example, with thyroid cancer.
If the clinical presentation is consistent with hypothyroidism, the clinician needs to consider secondary hypothyroidism and the most reliable test to confirm this diagnosis is a low T4 level since TSH levels can be normal or elevated due to a bioactive isoform of TSH.
Also, patients on steroids, dopamine, and somatostatin analogs, or those with sick euthyroid syndrome can have low TSH levels.
In the first trimester of pregnancy when HCG levels peak, TSH levels can be low since HCG can engage the TSH receptor and activate the thyroid possibly resulting in gestational hyperthyroidism. Also, TSH is an important screening test in neonates to diagnose hypothyroidism and prevent complications such as intellectual impairment.
When used in conjunction with physical exam and history, the TSH level can help determine the cause of hypothyroidism or hyperthyroidism.
Symptoms of hyperthyroidism include increased metabolic rate, weight loss, negative nitrogen balance, increased heat production, excessive sweating, increased cardiac output, dyspnea (shortness of breath), tremor or muscle weakness, exophthalmos, and goiter.
When a patient exhibits these symptoms, a decreased TSH would be indicative of feedback inhibition of T3 on the anterior lobe; while an increased TSH would be indicative of a defect in the anterior pituitary.
Hyperthyroidism can be caused by Graves' disease in which there is an increased thyroid-stimulating immunoglobulin, thyroid neoplasm (for example, toxic adenoma), excess TSH secretion, or exogenous T3 or T4.
Treatment for this should include propylthiouracil (which inhibits peroxidase enzyme and thyroid hormone synthesis), thyroidectomy, radioiodine therapy which destroys the thyroid, and beta-adrenergic blocking agents (adjunct therapy).
Symptoms of hypothyroidism include decreased basal metabolic rate, weight gain, and nitrogen balance, decreased heat production, cold sensitivity, decreased cardiac output, hypoventilation, lethargy and mental slowness, drooping eyelids, myxedema, growth retardation, mental retardation in perinatal patients, and goiter. When a patient exhibits these symptoms, an increased TSH would indicate negative feedback if the primary defect is in the thyroid gland; while a decreased TSH would be indicative of a defect in the hypothalamus or anterior pituitary. Hypothyroidism can be caused by thyroiditis (autoimmune or Hashimoto thyroiditis), surgery for hyperthyroidism, iodine-deficiency, congenital (cretinism), or decreased TRH or TSH. Treatment for this should include thyroid hormone replacement.
To access free multiple choice questions on this topic, click here.
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Understanding thyroid tests
Created: May 24, 2011; Last Update: April 30, 2018; Next update: 2021.
The thyroid gland is a vitally important endocrine (hormone) gland that is mainly involved in the body’s energy metabolism. It is located at the front of the neck, below the voice box, and is butterfly-shaped. The thyroid gland produces the thyroid hormones triiodothyronine (T3) and thyroxine (T4), among other things.
These thyroid hormones have various functions: They are responsible for the metabolism, growth and development of the body. The production of the thyroid hormones is regulated by the pituitary gland. The pituitary gland makes a hormone called TSH (thyroid-stimulating hormone). TSH not only stimulates the production of thyroid hormones – it also influences the size of the thyroid gland.
The production of TSH, in turn, is inhibited by thyroid hormones. The system can be compared to a thermostat, which makes sure that the room is kept at a certain temperature. So the concentration of thyroid hormones in the blood is usually fairly constant.
There are different tests and examinations to check whether the thyroid gland is functioning normally and whether its surface, shape and size are normal.
In this examination, the doctor feels the neck with his or her hands, paying attention to what the thyroid gland feels and whether it is enlarged.
An enlarged thyroid – also called a goiter – can be a sign of an iodine deficiency that hasn't yet affected the function of the thyroid. But it could also be a sign of an overactive thyroid (hyperthyroidism) or an underactive thyroid (hypothyroidism), where too many or too few hormones are made respectively.
Nodules that can be felt from the outside may also be a sign of a thyroid problem. But sometimes people have an enlarged thyroid gland or nodules without it affecting the function of their thyroid gland.
So this palpation examination can only tell us whether there might be a thyroid problem. Further tests and examinations are needed in order to be sure.
The thyroid gland constantly releases a certain amount of hormones into the blood. So a blood test can be used to determine the amounts of hormones produced by the thyroid gland.
The blood test measures the levels of TSH and the thyroid hormones triiodothyronine (T3) and thyroxine (T4). A change in the TSH level can be an early sign of a thyroid problem.
For this reason, it is common to only measure the TSH level at first.
If the TSH level in the blood is higher or lower than normal, the levels of the thyroid hormones T4 and T3 are also measured. Most thyroid hormones are bound to certain proteins in the blood. Only unbound “free” thyroid hormones are active and have an effect, though. So only the free thyroid hormones are measured (FT3 and FT4 – where “F” stands for “free”).
When trying to find out what is causing a thyroid problem, a blood test is done to look for thyroid antibodies. These antibodies are made if the immune system attacks the body’s own thyroid tissue by mistake. They may also block the effect of thyroid hormones.
Another hormone produced by the thyroid gland is called calcitonin. The level of calcitonin in the blood is usually only measured if there is reason to believe that someone has a certain type of thyroid cancer which increases the amount of calcitonin.
If the levels of T3 and T4 in the blood are too high or too low, there is an imbalance between the amount of thyroid hormones needed by the body and the amount of thyroid hormones available. The levels of the following substances can help find out what is causing the imbalance:
- Thyroid-stimulating hormone (TSH): High TSH levels are a sign of an underactive thyroid (hypothyroidism). The pituitary gland produces more TSH in order to stimulate the thyroid gland to produce thyroid hormones. Very low TSH levels in the blood may be a sign of an overactive thyroid (hyperthyroidism). The pituitary gland then produces less TSH, in order to stop “telling” the thyroid gland to make more hormones.
- Free triiodothyronine (FT3) and free thyroxine (FT4): High levels of free thyroid hormones in the blood may be a sign of an overactive thyroid, and low levels could be a sign of an underactive thyroid.
- Thyroid antibodies: The concentration of thyroid antibodies in the blood is higher in certain disorders where the body’s immune system attacks the thyroid gland. These include Hashimoto’s disease and Graves’ disease. Low levels of thyroid antibodies may be a sign of various diseases, such as an inflammation of the thyroid gland (thyroiditis), type 1 diabetes or rheumatoid arthritis.
- Calcitonin: Calcitonin levels are usually higher in a certain type of thyroid cancer. But high levels of calcitonin can also be a sign of other diseases, such as kidney failure. Calcitonin levels play an important role in calcium and bone metabolism too.
The concentration of TSH and thyroid hormones in the blood can also be influenced by the long-term use of certain medications. These medications include:
- Acetylsalicylic acid (ASA, the drug in medicines Aspirin)
- St John's wort
- Certain diuretic medications containing furosemide
- Thyroid medications
Because of this, it’s important to let your doctor know about any medications you are taking before having a blood test.
In a thyroid ultrasound (sonography), sound waves are sent to the thyroid gland. Depending on the type of tissue they bounce off there, the sound waves are then sent back with different intensities or not at all.
To do the examination, a small amount of gel is put on the “head” (transducer) of the ultrasound device, which is then moved over the neck.
The sound waves that bounce off the thyroid tissue are measured by the transducer and turned into a spatial image that is shown on a screen.
The ultrasound image shows whether the thyroid gland is enlarged. Changes in the tissue – cysts or age-related changes in its structure – can also be seen. An enlarged thyroid gland could be a sign that it is underactive or overactive.
To know for sure whether the thyroid gland really is making too many hormones or not enough, a blood test has to be done too. If nodules (lumps) are discovered in the ultrasound examination, other examinations may be done to find out more about them. These include a thyroid scan or – in some cases – magnetic resonance imaging (MRI).
A thyroid scan (or thyroid scintigraphy) is an imaging technique used to see how active the thyroid gland is (the amount of hormones it is producing). Before doing the scan, a slightly radioactive substance is injected into an arm vein.
This substance travels around the body in the bloodstream, but most of it is absorbed by the thyroid gland. More active areas of the thyroid gland absorb more of the substance, and less active areas absorb less.
The thyroid scan image shows how much of the radioactive substance has been absorbed in different areas of the thyroid gland. This image is called a scintigram.
It may be necessary to stop taking certain drugs, such as thyroid medications, before having a thyroid scan. Because of this, it’s important to let your doctor know about any medication you are taking.
Thyroid scans can have adverse effects: In rare cases, the needle might damage blood vessels or nerves, or the skin at the site of injection may become inflamed. Allergic reactions, particularly to the injected substance, are possible.
People are exposed to a small amount of radiation during the scan. Only very small amounts of radioactive substances are used, though, and they are broken down in the body within a few days.
Thyroid scans allow us to look at how active the thyroid tissue is: The more active it is, the more blood goes through it and the more of the injected substance builds up in it. Active areas of the thyroid gland can be clearly seen on the thyroid scan image.
Depending on how much of the injected substance builds up, “cold” nodules and “hot” nodules can be identified:
Cold nodules have less of the radioactive substance in them because the metabolism in their tissue is slower (less active). In most cases, cold nodules are caused by harmless changes in the tissue. In very rare cases, though, they are caused by a thyroid tumor.
Hot nodules have more of the radioactive substance in them – their metabolism is faster (more active) and their tissue produces more hormones. If hot nodules grow bigger than a certain size, they may lead to an overactive thyroid.
In fine needle aspiration, a very fine, hollow needle is inserted into the thyroid gland to remove samples of tissue or fluid. It’s usually not necessary to numb the area with an anesthetic because it’s not more unpleasant than having a normal blood sample taken from an arm. To be able to see the procedure better, doctors often use an ultrasound machine too.
In rare cases, the place where the needle was inserted may become bruised or inflamed. If you take medication that stops blood from clotting (anticoagulants), it’s important to talk to your doctor about whether you should stop taking it before the procedure.
Fine needle aspiration can provide further information about whether the changes in thyroid tissue are benign (non-cancerous) or malignant (cancerous).
The tissue samples that are taken are sent to a laboratory, where the cells are examined. Fine needle aspiration can be used to remove fluid from fluid-filled cysts too.
Removing and examining thyroid tissue in this way also allows doctors to see whether the tissue is inflamed.
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Thyroxine (T4) Test: MedlinePlus Lab Test Information
URL of this page: https://medlineplus.gov/lab-tests/thyroxine-t4-test/
A thyroxine test helps diagnose disorders of the thyroid. The thyroid is a small, butterfly-shaped gland located near the throat. Your thyroid makes hormones that regulate the way your body uses energy.
It also plays an important role in regulating your weight, body temperature, muscle strength, and even your mood. Thyroxine, also known as T4, is a type of thyroid hormone. This test measures the level of T4 in your blood. Too much or too little T4 can indicate thyroid disease.
The T4 hormone comes in two forms:
- Free T4, which enters the body tissues where it's needed
- Bound T4, which attaches to proteins, preventing it from entering body tissues
A test that measures both free and bound T4 is called a total T4 test. Other tests measure just free T4. A free T4 test is considered more accurate than a total T4 test for checking thyroid function.
Other names: free thyroxine, free T4, total T4 concentration, thyroxine screen, free T4 concentration
A T4 test is used to evaluate thyroid function and diagnose thyroid disease.
Thyroid disease is much more common in women and most often occurs under the age of 40. It also tend to run in families. You may need a thyroxine test if a family member has ever had thyroid disease or if you have symptoms of having too much thyroid hormone in your blood, a condition called hyperthyroidism, or symptoms of having too little thyroid hormone, a condition called hypothyroidism.
Symptoms of hyperthyroidism, also known as overactive thyroid, include:
- Weight loss
- Tremors in the hands
- Increased heart rate
- Bulging of the eyes
- Trouble sleeping
Symptoms of hypothyroidism, also known as underactive thyroid, include:
- Weight gain
- Hair loss
- Low tolerance for cold temperatures
- Irregular menstrual periods
A health care professional will take a blood sample from a vein in your arm, using a small needle. After the needle is inserted, a small amount of blood will be collected into a test tube or vial. You may feel a little sting when the needle goes in or out. This usually takes less than five minutes.
You don't need any special preparations for a thyroxine blood test. If your health care provider has ordered more tests on your blood sample, you may need to fast (not eat or drink) for several hours before the test. Your health care provider will let you know if there are any special instructions to follow.
There is very little risk to having a blood test. You may have slight pain or bruising at the spot where the needle was put in, but most symptoms go away quickly.
Your results may come in the form of total T4, free T4, or a free T4 index.
- The free T4 index includes a formula that compares free and bound T4.
- High levels of any of these tests (total T4, free T4, or free T4 index) may indicate an overactive thyroid, also known as hyperthyroidism.
- Low levels of any of these tests (total T4, free T4, or free T4 index) may indicate an underactive thyroid, also known as hypothyroidism.
If your T4 test results are not normal, your health care provider will ly order more thyroid tests to help make a diagnosis. These may include:
- T3 thyroid hormone tests. T3 is another hormone made by the thyroid.
- A TSH (thyroid stimulating hormone) test. TSH is a hormone made by the pituitary gland. It stimulates the thyroid to produce T4 and T3 hormones.
- Tests to diagnose Graves' disease, an autoimmune disease that causes hyperthyroidism
- Tests to diagnose Hashimoto's thyroiditis, an autoimmune disease that causes hypothyroidism
Thyroid changes can happen during pregnancy. Although it is not common, some women can develop thyroid disease during pregnancy. Hyperthyroidism happens in about 0.1% to 0.4% of pregnancies, while hypothyroidism happens in approximately 2.5% of pregnancies.
Hyperthyroidism, and less often, hypothyroidism, may remain after pregnancy. If you develop a thyroid condition during pregnancy, your health care provider will monitor your condition after your baby is born. Also, if you have a history of thyroid disease, be sure to talk with your health care provider if you are pregnant or are thinking of becoming pregnant.