The term goiter identifies an increase in the volume of the thyroid gland. This enlargement of the gland can be a passing disorder or a symptom of a more serious disease. In any case, the final result is the appearance of a more or less conspicuous bump on the neck.
First of all, it is appropriate to distinguish the various types of goiter and the causes that determine its onset.
First, based on the functional state of the thyroid, goiter can be toxic or non-toxic. To better understand this distinction, it should be noted that the enlargement of the thyroid gland can be accompanied, or not, by alterations in the functionality of the gland, which can be increased (and in this case we are talking about hyperthyroidism) or decreased (and in this case we speaks of hypothyroidism). When we talk about toxic goiter, it means that thyroid enlargement is associated with hyperthyroidism.
Having ascertained that goiter can occur both in conditions of hyperthyroidism and in conditions of hypothyroidism, there are, however, also goiters that do not modify the thyroid function at all. The latter are called non-toxic goiters or simple goiters and consist of swellings that cannot be referred to either hyperthyroidism or hypothyroidism or even to increases in volume of an inflammatory or tumor nature.
If from the functional point of view we are talking about simple goiters and toxic goiters, from the morphological point of view it is possible to distinguish diffuse goiters and nodular goiters.
We speak of diffuse goiter when the whole thyroid increases its size uniformly and does not have nodules. When, on the other hand, the goiter is characterized by one or more circumscribed swellings, similar to small lumps or protuberances, it is called a nodular goiter. In particular, we are talking about uninodular goiter if there is only one nodule and multinodular goiter, if two or more nodules are present.
Often the multinodular goiter represents the natural evolution of a simple goiter. In some cases, in fact, the chronic stimulation of the thyroid gland, with relative increase in the homogeneous volume of the gland, ends up selecting groups of cells that begin to develop in an accelerated way and form more nodules. Recall that these nodules can grow and produce thyroid hormones on their own. In other words, they behave like a toxic goiter and, after some time, can lead to hyperthyroidism.
Goiter can be caused by a number of factors.
Among the external causes, therefore among the exogenous causes, the best known and most common is the lack of iodine in drinking water and food; in these cases we speak of endemic goiter. This type of goiter is called "endemic" because it is widespread in specific geographical areas, especially mountainous and far from the sea, or in populations that lead a diet poor in iodine or rich in foods, called "gozzigeni", which hinder its assimilation (among goitigenic foods, I remind you of cabbage, onion, turnip and even soy consumed in large quantities).
In the case of endemic goiter, the enlargement of the thyroid therefore represents a compensation phenomenon for iodine deficiency. As we saw in a previous video, in fact, iodine is essential for the synthesis of thyroid hormones, which are thyroxine and triiodothyronine. Since these hormones are deficient, the pituitary gland picks up this deficit and stimulates the activity of the thyroid by secreting the thyroid stimulating hormone. As a result of this hormone, also known as TSH, the thyroid becomes more active to try to produce quantities of hormones adequate to the needs of the body. As a result, the follicular cells produce large quantities of thyroglobulin, but given the iodine deficiency they are unable to combine them with this mineral to form the hormone in a definitive and functional form. This results in a further increase in TSH levels, the thyroid gland works harder and swells, giving rise to goiter.
In the presence of iodine deficiency, the massive administration of the mineral through supplements or food may not solve the problem. In fact, it can cause opposite effects, ie hyperthyroidism following the massive conversion of all previously synthesized thyroglobulin into functioning thyroid hormones. That is why, to prevent iodine deficiency diseases, iodine prophylaxis is important, where the simple integration of iodine in the diet may be sufficient to reduce its incidence. The most effective and economical method to ensure the correct daily intake of iodine is to use iodized salt instead of traditional table salt. But let's go back to the other possible situations that cause goiter.
After having seen the exogenous causes, therefore external, let's move on to the endogenous causes, that is internal to the organism. Among these, the most important cause consists of congenital defects related to the process of synthesis of thyroid hormones. These alterations can be responsible for the repetition, in the In the family context of cases of hereditary goiter Some examples include deficiencies in iodine metabolism, thyroglobulin synthesis or thyroid hormone deiodation, ie peripheral conversion of thyroxine T4 to triiodothyronine T3.
Goiter can also be caused by drugs, particularly those that affect thyroid activities, such as thyroid drugs. As we have seen, goiter can also be the result of an excessive intake of iodine. Other possible causes of goiter are inflammations that develop in the thyroid, such as Hashimoto's thyroiditis, and tissue proliferation of tumor origin.
Finally, it is important to take into account that the thyroid gland can grow transiently, therefore for a limited period, even in the presence of particular physiological conditions and in periods of greater work of the gland, such as during puberty, pregnancy or menopause.
As for the symptoms of goiter, there are some common ones, therefore identical in all the various forms of goiter and other signs that, on the other hand, are specific to the pathologies that cause it.
Starting from the common symptoms, as we have seen, the thyroid goiter manifests itself with a swelling of the anterior region of the neck, which can be more or less uniform and more or less evident. In other words, it can take on the appearance of a small lump or a billiard ball. If the increase in volume is excessive, it can be an aesthetic problem and the mass can compress the underlying trachea and esophagus. As it is easy to guess, this can cause hoarseness, problems in swallowing, a feeling of suffocation and difficulty in breathing.
When, on the other hand, the increase in size of the thyroid is caused by hyperthyroidism or hypothyroidism, the set of symptoms is characteristic of the underlying disease. To learn about the symptoms of hyperthyroidism and hypothyroidism, I refer you to the relative lessons that you can always find on the My-personaltrainer.it website in the area dedicated to the Destination Wellness program.
The initial diagnostic classification of goiter problems is done by combining clinical observation with specific blood tests. The increase in the volume of the thyroid gland can, in fact, be assessed with an inspection of the neck and palpation of the gland by expert hands, while blood tests investigate thyroid function. Blood tests generally include the measurement of thyroid hormones and TSH. Since some cases of goiter have autoimmune causes, specific antithyroid antibodies characteristic of Hashimoto's thyroiditis or Graves' disease can also be looked for in the blood.
The instrumental tests performed most frequently in the case of goiter are ultrasound and thyroid scintigraphy. Ultrasound allows you to obtain an image of the thyroid, which is very useful for assessing the size and the possible presence of cysts or nodules. Scintigraphy, on the other hand, is able to detect the hypo- or hyper-functioning of any identified nodules. If these nodules appear "suspicious", therefore at potential tumor risk, the needle aspirate (ie thyroid biopsy) allows us to clarify the nature of the nodule itself.
The treatment of goiter depends on the functional state of the thyroid, that is, on whether the gland is overactive or not, and on the size of the goiter.
Therapy is not necessary when the goiter is small in size and is not associated with functional alterations of the thyroid; in these cases, TSH levels are normal and the patient is asymptomatic. In other cases, if the thyroid gland is hypofunctional or hyperfunctioning, treatment is aimed primarily at the underlying pathology. In most of these cases, drug or metabolic radiotherapy allows for a gradual reduction of goiter.
When the thyroid enlargement reaches excessive dimensions and in the presence of toxic nodular goiters, it is possible to resort to surgery to partially or totally remove the gland. This intervention allows to restore normal aesthetics, but also to prevent any compressive phenomena.
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