The thyrotoxicosis It is the set of symptoms and clinical signs derived from high levels of circulating thyroid hormone in the blood. In some cases it is used as a synonym for hyperthyroidism; strictly speaking they are two different conditions although associated.
Hyperthyroidism is defined as high levels of thyroid hormone in the blood. However, not all patients with this pathology present clinical signs, hence the classification of hyperthyroidism into clinical and subclinical.
In subclinical hyperthyroidism, the thyroid hormone levels in the blood are elevated but the patient does not present any particular symptoms. On the other hand, in clinical hyperthyroidism, in addition to elevated hormonal levels, symptoms of hyperthyroidism also occur.
Some authors even make the difference between hyperthyroidism and thyrotoxicosis on the basis of the intensity of the symptoms. Thus, according to this current of thought, patients with clinical hyperthyroidism are those with high levels of thyroid hormone and mild or easily treatable symptoms..
On the other hand, those cases with very severe symptoms or that do not respond to treatment are classified as thyrotoxicosis..
Although this differentiation is used by some authors, it is artificial since the severity of the symptoms may increase over time or even vary both more and less throughout the evolution in the same patient..
Thus, for practical purposes it can be concluded that clinical hyperthyroidism is synonymous with thyrotoxicosis since elevated levels of T3 and T4 (thyroid hormones) will sooner or later have significant effects on the health of the person..
Article index
The thyroid gland regulates a wide range of body functions through its hormones, its effect generally being to stimulate the function of the target organs..
Due to this, when thyroid hormone levels rise above normal, its stimulating effect is enhanced, presenting the following symptoms:
- Anxiety and / or agitation
- Insomnia
- Tachycardia (associated or not with palpitations)
- Arterial hypertension
- Exophthalmos
- Weightloss
- Hair loss and nail thinning
Anxiety, agitation and insomnia are due to the stimulating effect of thyroid hormone on the central nervous system, while tachycardia and arterial hypertension are due to its positive regulatory effects on the heart (positive inotropic effect) and blood vessels (vasoconstriction ).
Exophthalmos is due to the proliferation of retroocular tissues in response to high levels of thyroid hormone, leaving less space in the orbits for the eyes, which seem to "go out" of their place, a situation that is often known colloquially as "bulging eyes. ".
For its part, weight loss as well as hair loss and thinning of the nails is due to the catabolic effect of thyroid hormone; therefore, the body's nutritional reserves are “burned” to produce the fuel that the body requires to function at full throttle.
The causes of thyrotoxicosis are multiple and varied, however they can be divided into four large groups according to the pathogenesis:
- Overproduction of thyroid hormone
- Destruction of thyroid tissue
- Ectopic thyroid hormone production
- Exogenous thyroid hormone intake
Although all the causes converge in a common end that is the elevation of the circulating levels of thyroid hormones (T3 and T4), the pathophysiological mechanism by which they arrive there (and therefore the treatment) differs markedly.
There are multiple conditions in which an excessive amount of thyroid hormone is produced, but they all coincide in a common point: the follicular cells of the thyroid work more than normal, producing more thyroid hormone than the body needs..
The most common causes of thyroid hormone overproduction are:
- Graves-Basedow disease
- Toxic goiter
- Toxic thyroid adenoma
- Hyperthyroidism secondary to elevated TSH
To understand the treatment of these pathologies, it is necessary to remember their basic characteristics a little:
It is the most common cause of hyperthyroidism.
It is an autoimmune disease whose pathophysiology is not fully understood. To date, it is known that there are antibodies that bind to the TSH receptor, stimulating the thyroid gland, which therefore produces excessive levels of thyroid hormone..
This is due to the fact that the stimulation by autoantibodies escapes the negative regulation that high levels of T3 and T4 have on the thyroid itself, so the gland keeps producing hormones in a sustained and uncontrolled way..
It is a diffuse increase in the thyroid gland with expansion of the cell mass, which results in a larger gland with a greater capacity to produce thyroid hormone..
It may or may not be a multinodular goiter, but in both cases the entire gland functions above the normal level. Consider that there is a goiter associated with hypothyroidism as well, in these cases the pathophysiology is totally different.
In these cases, it is a thyroid nodule that escapes normal regulatory mechanisms and begins to produce thyroid hormone at levels higher than normal..
This production of thyroid hormone not only stimulates the target organs (producing thyrotoxicosis), but also inhibits healthy thyroid tissue so that the nodule assumes complete control of the thyroid.
They are benign lesions but with high morbidity rates due to their effects on metabolism.
The pituitary gland and the thyroid are chemically interconnected and mutually regulate. Thyroid stimulating hormone or TSH is produced in the pituitary gland, which stimulates the thyroid.
In turn, thyroid hormone inhibits the production of TSH in the pituitary gland..
When pituitary adenomas develop that cause an uncontrolled elevation of TSH, the negative feedback mechanism is lost. Therefore, the thyroid is forced to work harder than normal by sustained elevated TSH levels, since adenomas do not respond to negative feedback from T3 and T4..
The thyroid functions as both a synthesis and storage site for thyroid hormone..
When the thyroid tissue is injured, this reservoir opens and releases the thyroid hormone stored there into the bloodstream, raising its levels above normal..
This is precisely what happens in certain autoimmune diseases, such as Hashimoto's thyroiditis, where antibodies destroy the thyroid gland causing all of its T3 and T4 stores to be suddenly released into the blood..
Unlike cases in which more thyroid hormone is produced than normal, when the thyroid tissue is destroyed, hormonal stores are released, but the synthesis capacity of the gland is also compromised..
In this way, as the disease progresses, hormonal reserves are depleted and the gland produces less and less (due to the loss of follicular cells). Therefore, the patient presents a first phase of hyperthyroidism, which transiently normalizes to finally end in hypothyroidism.
It is a rare but real cause. These are ovarian tumors (ovarian struma) that have the ability not only to produce thyroid hormone, but to do so without any control of the negative feedback mechanisms that are normally involved in its synthesis..
Due to this, thyroid hormone levels rise steadily and steadily, which in turn inhibits TSH secretion and therefore stimulates it on the thyroid, which is literally "turned off".
It is not considered hyperthyroidism or thyrotoxicosis itself, however the effects on the body are the same.
Sometimes thyroid hormone overdose is due to an inadequate adjustment of the initial dose, while in others it may be due to the use of these hormones to induce catabolism (something for which they are not approved).
In any case, the exogenous thyroid hormone levels induce a clinical picture indistinguishable from real hyperthyroidism, with the difference that it can be treated much more easily.
Regardless of the cause, thyrotoxicosis can be divided into two large groups: primary and secondary.
This group includes all those entities where the problem begins in the thyroid, so that Graves-Basedow disease, toxic goiter and toxic thyroid adenomas fall into this category..
The same could be said for thyroiditis, since the problem that causes elevated thyroid hormone levels occurs in the thyroid gland.
For its part, thyrotoxicosis is considered to be secondary when the cause lies beyond the thyroid.
Thyrotoxicosis is therefore considered secondary to that which occurs due to elevated TSH production, as well as those cases of ectopic thyroid hormone production. In both situations the cause of the problem is outside the thyroid.
The treatment of thyrotoxicosis will depend largely on the cause, the age of the patient and the associated clinical conditions..
From a pharmacological point of view, there are therapeutic measures aimed at reducing the impact of excess thyroid hormone on the target organs. Such is the case of beta-blockers, which are used to treat tachycardia and hypertension induced by hyperthyroidism..
On the other hand, there are medications such as propylthiouracil and methimazole whose objective is to decrease the production of thyroid hormone to keep its levels within normal limits..
These drugs are usually very effective, however when they fail to control the problem, it is necessary to use ablative methods such as total thyroidectomy (indicated in toxic goiter refractory to treatment) or treatment with radioactive iodine (frequently used in the disease of Graves-Basedow).
In addition to therapeutic measures aimed at treating the thyroid (either pharmacologically or by ablation), there are specific treatment strategies for particular situations.
Thus, in cases of ovarian struma, oophorectomy is indicated, while in TSH-producing pituitary adenomas, specific pharmacological treatment or even surgery to remove said adenoma may be indicated..
In cases of thyroiditis, one must be very cautious in the choice of treatment, since they are self-limited processes in time; hence the need to carefully evaluate the long-term benefits of medical treatment and compare them with surgical resolution.
Finally, when thyrotoxicosis is due to excessive intake of exogenous thyroid hormone, dose adjustment turns out to be the ideal treatment..
Yet No Comments