There thyroid and the gland largest endocrine in the human body, it is located in the neck and has a bilobed shape, similar to a butterfly. The thyroid gland is made up of cells called thyrocytes, which produce two main types of hormones: the thyroid hormones properly called, and calcitonin.
The thyroid hormones are iodothyronines triiodothyronine (T3) and tetraiodothyronine or thyroxine (T4), which regulate normal cell growth and differentiation in the early stages of life and energy and metabolic balance in adults. Calcitonin is a substance that regulates the balance of calcium and phosphorus concentrations in the blood, and is used as a tumor marker for medullary thyroid tumors.
What is the thyroid gland?
The thyroid is a very important endocrine gland for the body, it is regulated bythyrotropic hormone (TSH) produced by the pituitary, and in turn produces gli thyroid hormones T3 and T4, essential for life. The thyroid in adults is shaped like a butterfly and is located on the neck in front of the trachea.
The thyroid adheres to the trachea and the overlying thyroid cartilage thanks to a median and two lateral ligaments that allow it to follow the swallowing movements. The two thyroid lobes lateral are connected by a portion of tissue called isthmus. It is curious to note that, in nearly half of people, there is an additional lobe called pyramidal lobe, an unequal structure located medially, extending from the isthmus upwards, which is nothing more than a remnant of the thyroglossal duct, a structure present during development.
Typically, two smaller glands called adherent posterior to each of the two thyroid lobes parathyroid glands (the parathyroid glands are four in total, two upper and two lower, producing a substance called parathyroid hormone). Two nerves pass under the thyroid, between the thyroid and the trachea, called recurrent laryngeal nerves.
In the normal adult the weight of the thyroid varies from 15 to 25 g depending on the body mass of the person; its dimensions are about 2.5-4 cm in height, a couple of centimeters in width for each lobe and a thickness ranging from 1 cm to 1.5 cm.
The thyroid is nourished by lower thyroid arteries (branch of the subclavian artery) and from upper thyroid arteries (branch of the carotid artery), and constitutes one of the most supplied tissues in the whole body.
The thyroid is formed by follicles, closely joined structures of 0.1-0.5 mm in diameter, surrounded by a thick branching of adrenergic nerve endings. The peripheral border of the follicle is made up of a thin layer of epithelial cells, called follicular cells, which determine the lumen in which thyroglobulin is deposited.
Under the stimulus of thyrotropin the follicular cells enlarge, they begin to collect the iodine found circulating in the blood, with which they iodize thyroglobulin, a protein previously produced and stored in the follicular lumen. From the iodation process of thyroglobulin, thyroid hormones are synthesized thanks to specific enzymes including thyroperoxidase
In the thyroid there are also C cells or parafollicular cells, which have the function of synthesizing calcitonin, a substance that regulates the metabolism of calcium-phosphorus.
Thyroid and iodine metabolism
Iodine is a trace element that is taken with food and water in the form of iodide.
According to the WHO (i.e. WHO, the World Health Organization) considers recommended an iodine intake of 50-100 µg (micrograms) in infancy, 150 µg for adults and 200 µg for pregnant women .
The iodide is transported in the bloodstream to the thyroid cells (the cells that make up the thyroid) thanks to a protein located on the basement membrane of the thyroid cell.
In the upper part of the thyroid cell, a second transport protein carries the iodine towards the colloid where the actual hormonal production takes place.
Inside the thyroid the concentration of iodine reaches a quantity 10,000 times greater than that present in foods normally introduced with the diet
Inside the thyroid cell, iodide is organized into hydrogen peroxide (H.2OR2) through the enzyme TPO (thyroperoxidase) thus allowing the inclusion of tyrosine residues of thyroglobulin. This reaction is also stimulated by thyroglobulin.
The total of organified iodine is about 7-12 mg and represents a form of deposit of precursors (molecules that could give rise to thyroid hormones) but also of real thyroid hormones.
About 75 µg of iodide are released into the bloodstream every day: Iodine circulates bound to specific carrier proteins. Of the 75 µg released into the circulation every 24 hours, about 55 µg return to the thyroid iodide pool, while the other 20 µg are conjugated with glucuronide and eliminated in the faeces. Most of the dietary iodide is instead eliminated in the urine: for this reason the measurement of urinary iodine (ioduria) is a fairly reliable marker of the dietary indic intake.
What happens if the body takes too much or too much iodine (for example if it becomes intoxicated with drugs with Eutirox?). Fortunately, the thyroid has a self-regulating mechanism due to excess iodine and / or thyroid hormones.
The organism in fact responds with:
- Wolff-Chaikoff mechanism: blocking the iodation of thyroglobulin and therefore of the production of thyroid hormones. The Wolff-CHaikoff effect is transient and resolves days / weeks after the normalization of iodine intake.
- Reduction of the stimulating effect of TSH on the thyroid.
- Diminished metabolism of thyroglobulin present in the follicles decreases, resulting in a decrease in the production of thyroid hormones.
Thyroid and thyroid hormones
The human thyroid, as already mentioned, produces two metabolically active hormones: T4, thyroxine or tetraiodothyronine, and T3 or triiodothyronine.
The synthesis of thyroid hormones requires some main actors, namely it iodine, the thyroglobulin and the enzyme thyroid peroxidase.
The synthesis of thyroid hormones occurs through six basic steps:
- active transport of iodide across the basement membrane of the thyroid cell;
- oxidation of iodide to iodine;
- iodation of the tyrosine residues of the thyroglobulin protein;
- coupling of tyrosine residues within thyroglobulin with the formation of triiodothyronine and thyroxine;
- proteolysis (ie breaking of protein bonds) of thyroglobulin with release of T3 and T4 into the circulation;
- desiodation of the colloid left inside the thyroid cell to be able to use the iodine again.
Let's see in detail the role of thyroglobulin in this process.
What is Thyroglobulin and what role does it play in the formation of thyroid hormones? The synthesis of thyroid hormones occurs in thyroglobulin (often indicated by the abbreviation Tg).
Thyroglobulin is a protein produced and secreted only by follicular cells, it represents an index of activity of the thyroid gland and, not surprisingly, is also used as a tumor marker.
The iodide captured by the cell is "activated" by the thyroid peroxidase (TPO) in a process called iodine organization: in a nutshell, the thyroid residues of thyroglobulin are iodized, thus forming the mono-iodiotyrosine precursors (MIT) and diiodotyrosine (DIT), which combined with each other will give thyroid hormones T3 o triiodothyronine (MIT + DIT) e T4 or thyroxine (DIT + DIT).
There thyroxine, in turn, it can be enzymatically desiodated giving rise to the formation of two different isoforms of the triiodiotyrosine, of which 3,5,3'-T3 represents the biologically active form, while 3,3 ', 5'-T3, that is the reverse T3 or rT3) is metabolically inactive. Monoiodiotyrosine and diiodiotyrosine are normally circulating in very low quantities, they degrade in a short time and are physiologically innative.
What is the supply of thyroid hormones in our body? The thyroid contains a deposit of hormones equal to about 3-4 mg, equivalent to the requirement of about 1 month and an iodine supply equal to about 8-10 mg, which is sufficient for 2-3 months.
Effect of thyroid hormones
The effects induced by thyroid hormones are distinguished in early, present within hours, and delayed, which begin 4-6 hours after the activation of the peripheral thyroid hormone receptors and which are maintained for days.
The early effects of thyroid hormones I'm:
- increased intracellular transport of glucose
- increased transport of amino acids in various body tissues such as myocardiocytes (heart muscle cells), thymocytes (thymus cells) and chondrocytes (cartilage-forming cells).
The main late effects of hormones thyroxine and triiodothyronine on our body are instead:
- stimulation of fetal development
- increased tissue oxygen consumption (O2)
- thermogenesis (heat production)
- inotropic effect (increased contractile force of the heart)
- chronotropic effect (increased heart rate)
- increase in the number and state of activation of adrenergic receptors in heart muscle, skeletal muscle, adipose tissue (body fat) and lymphocytes
- increased respiratory rate by activating the breath center
- activation of erythropoiesis) process of formation of erythrocytes, i.e. red blood cells)
- increased intestinal motility
- increase in skeletal turnover, i.e. the process of bone replacement
- synthesis of structural proteins of the central nervous system (CNS), allowing its normal development and function
- increased hepatic gluconeogenesis (formation of glucose in the liver)
- increase in glycogenolysis (process of degradation of glycogen, the main deposit of glucose, with an increase in blood sugar
- increased absorption of glucose in the intestine
- increased metabolic turnover both of many hormones and of pharmacological substances
Thyroid diseases: most frequent problems and pathologies
The thyroid gland can be affected by numerous pathologies, which affect its physical structure (enlargement, atrophy, formation of thyroid nodules benign or malignant in it) and its hormonal secretory function (hypofunction or hypothyroidism, hyperfunction or hyperthyroidism).
THE thyroid disorders fortunately they are often symptomatic from their onset, allowing for a quick and effective diagnosis. In the case of thyroid malfunction, autoimmune thyroid disease is often present. Less frequently there are other pathologies: let's see in detail what are the main diseases that can affect the thyroid:
Diseases with normal thyroid function (euthyroidism):
- Diffuse eumetabolic or non-toxic goiter, may be sporadic or endemic
- Uninodular goiter or non-toxic multinodular goiter, also may be sporadic or endemic
- Transient physiological goiter: can be found in physiological situations such as menarche, pregnancy, and menopause
- Transient iatrogenic goiter, caused by taking drugs containing excess thyroid hormones or iodine
- Transient goiter caused by dietary deficiency of iodine or by the intake of antithyroid substances
- Acute infectious or suppurative thyroiditis
- Subacute thyroiditis or De Quervain's thyroiditis in the euthyroid phase
- Diseases Hashimoto's thyroiditis or chronic autoimmune thyroiditis in the euthyroid phase
- Postpartum thyroiditis and silent thyroiditis in the euthyroid phase
- Chronic Riedel's thyroiditis
- Benign neoplasms
- Single thyroid nodule
- Malignant tumors
- Differentiated papillary carcinoma
- Differentiated follicular carcinoma
- Undifferentiated or anaplastic carcinoma
- Medullary carcinoma
Diseases with reduced thyroid function (hypothyroidism)
Primary adult hypothyroidism:
- chronic autoimmune thyroiditis with or without goiter
- iatrogenic hypothyroidism secondary to thyroidectomy, surgery in structures close to the thyroid, radiotherapy or radioiodine therapy
- diffuse and nodular hypofunctional goiter
- Advanced stage Basedow-Graves disease
- hypothyroidism due to iodine deficiency
Congenital neonatal hypothyroidism:
- thyroid dysgenesis / ectopia
- enzymatic defects of hormone synthesis
Secondary hypothyroidism or pituitary hypothyroidism
Tertiary hypothyroidism, hypothalamic or central hypothyroidism
Tissue peripheral resistance hypothyroidism thyroid hormones, receptor and / or post-receptor defects.
Diseases with thyrotoxicosis (hypermetabolism):
Thyrotoxicosis with hyperthyroidism, that is, with increased thyroid function
- Diffuse toxic hyperfunctioning goiter or Basedow-Graves disease
- Hyperfunctioning toxic multinodular goiter or Plummer's disease
- Hyperfunctioning toxic autonomous nodule
- Rare form thyrotoxicosis:
- excess of exogenous iodine,
- postpartum thyroiditis in the hyperthyroid phase,
- thyrotoxicosis due to pituitary resistance to thyroid hormones,
- TSH-secreting pituitary adenoma,
- hydatiform mole or choriocarcinoma,
- overproductive thyroid adenoma or follicular carcinoma
Thyrotoxicosis without hyperthyroidism, that is, without thyroid hyperfunction
- thyroid hormone-induced thyrotoxicosis (factitic and iatrogenic thyrotoxicosis)
- in thyroiditis in the thyrotoxic phase (post-inflammatory thyrotoxicosis or destruction of thyrocytes
- from amiodarone
- from metastases from thyroid cancer
- from struma ovarii
Many of the causes of thyroid disease listed above are actually very rare: let's say that in most cases thyroid problems are linked to the development of hypothyroidism following Hashimoto's thyroiditis, to the presence of hyperthyroidism secondary to Basedow-Graves' disease, to the finding of enlarged thyroid (goiter) or the presence of suspicious lumps for thyroid cancer.
Thyroid and symptoms
What are the main ones symptoms of thyroid malfunction? First of all, it should be clarified that the widespread term "thyroid symptoms " it makes no sense, since the thyroid is an organ which, when normal functioning, does not give any kind of symptomatology.
The situation is different in which this endocrine gland does not perform its regular function. If there is an overactive thyroid, the main result will be an increased production of thyroid hormones, a picture called by the medical definition of hyperthyroidism. Warning, hyperthyroidism is not synonymous with thyrotoxicosis: this last state in fact frames a situation of increased concentration of thyroid hormones in the blood, which is not necessarily a consequence of a thyroid dysfunction. In fact, just think of those who mistakenly take too high a dose of levothyroxine (Eutirox): they will certainly have a problem of thyrotoxicosis, but this is not linked to a picture of hyperthyroidism as the thyroid functions normally.
Having made this distinction, let's see which are the main ones symptoms of hyperthyroidism:
- tachycardia (increased heart rate)
- heart pounding (feeling of heart in the throat or butterflies in the chest),
- hypertension (increased blood pressure)
- mental instability with alternating crises of crying and laughter
- restlessness, nervousness, irritability
- tremor of the hands
- sleep disorders
- weakness (muscle weakness)
- myalgia (muscle pain)
- urticaria with rashes
- increased sweating
- increased appetite and thirst
- weight loss (weight loss, medically referred to as weight loss)
- loose stools and frequent discharge (diarrhea)
- disturbances of the menstrual cycle, with irregular cycles, menorrhagia or metrorrhagia or, in a minority of cases, disappearance of the menstrual cycle.
THE more frequent symptoms of hypothyroidism they are instead:
- weight gain (tendency to gain weight, with weight gain even in a few weeks)
- dry and brittle hair, which falls out more easily
- dry, pasty skin (myxedema)
- tendency to constipation (constipation)
- cold intolerance (people with hypothyroidism often admit that they are very cold)
- presence of nocturnal tingling and numbness in the hands and arms, due to an increased incidence of carpal tunnel syndrome
- hypoacusis (loss of hearing)
- menstrual cycle disorders with reduction or cycle or actual amenorrhea
- decreased libido (decreased sexual desire)
- asthenia, that is, great tiredness and exhaustion
- drop in heart rate (bradycardia)
- extrasystoles (abnormal heartbeats, "out of rhythm")
- dyslipidemias (increased cholesterol, hypertriglyceridaemia, reduction of HDL)
- lack of memory and concentration
- depressed mood, possible anxiety attacks and panic attacks
- personality change (e.g. from extrovert or introvert)
- apathetic facial expression (hypothyroid facies)
- epileptic seizures, psychiatric symptoms and hallucinations, psychiatric symptoms in what is called Hashimoto's encephalopathy are very rare
What are the blood tests to be performed to investigate the functioning of the thyroid gland? The main thyroid tests are the following:
- TSH or thyrotropin
- Total thyroxine or T4
- Free thyroxine or fT4
- Triiodothyronine or T3
- Free triiodothyronine or fT3
- Thyroid peroxidase or thyroid peroxidase antibodies (anti TPO)
- Antibodies anti thyroglobulin (anti Tg)
- TSH receptor antibodies (anti r-TSH)
To these tests are added some other analyzes that give an idea of the general functioning of our body, and which can help doctors identify the cause of any disorders that are also compatible with the symptoms of thyroid dysfunction:
- complete blood count with formula leukocyte
- sodium or Na
- potassium or K
- AST or GOT or aspartate aminotransferase
- ALT or GPT or alanine aminotransferase
- GGT or gama-glutamyl transpeptidase
- ALP or alkaline phosphatase
- total protein
- protein electrophoresis
- total cholesterol
- LDL cholesterol
- HDL cholesterol
In addition to blood tests, there are some diagnostic procedures that are very helpful in investigating the health of the thyroid gland. Thyroid ultrasound is the main diagnostic test, very simple to do and painless. If suspicious nodules are detected on ultrasound, a fine needle thyroid aspiration can be proceeded with, with the removal of a small peroption of thyroid tissue to be analyzed with the microscope.
To further investigate the investigation, it will be possible to perform a scintigraphy, which is a procedure that analyzes how a marked radiopharmaceutical concentrates in the thyroid gland, managing to identify any abnormal accumulations of tracer (hot nodules) or the complete, and in any case anomalous, absence accumulation (cold nodules).
As second-round examinations, CT (computerized axial tomography) is also very useful, not only to investigate the neck region but also to exclude, in the presence of a thyroid neoplasm, that there are secondary lesions (metastases) in other organs or systems .
Thyroid and therapies
Most thyroid pathologies have a specific and effective treatment. In case of reduced function of the thyroid cure it is essentially a replacement therapy with thyroid hormones administered in the form of a drug (tablets or drops). The most widely used active ingredient is levothyroxine (L-T4), an isoform of endogenous thyroxine, which many know by the name of Eutirox or Tirosint.
In the case of increased thyroid function (hyperthyroidism), the therapy is aimed at blocking the synthesis of thyroid hormones (Methimazole or Tapazole, Propylthiouracil or Periroid) or at controlling their action at the epripheric level (beta-blockers).
In acute or subacute thyroiditis, which can cause significant thyroid and peri-thyroid inflammation with swelling, redness and pain in the neck, therapy uses analgesic and antipyretic drugs (paracetamol) or anti-inflammatory drugs (ibuprofen, ketoprofen, naproxen, diclofenac and many others). In the most important cases, the doctor may recommend a short course of cortisone therapy to relieve symptoms and reduce inflammation in the thyroid (prednisone and beclomethasone the most used).
The drug therapy is completed by radioiodine (Iodine 131), which is usually used following a resective surgical therapy of a thyroid neoplasm, with the aim of both destroying any foci of residual thyroid cells that could not be removed during the operation. surgery, but also to highlight, thanks to a post-radioiodine scintigraphy, the position and extent of any residues.
The therapy of thyroid neoplasms makes use of the possibility of surgically eliminating part of the thyroid (hemithyroidectomy) or the whole gland (thiotal thyroidectomy) with possibly also afferent lymph nodes if necessary. Depending on the specific case, surgical therapy can also be accompanied by radiation therapy to "burn" any tumor cells still present and not resected because they are not visible.
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