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Thyroid hyperthyroidism - symptoms, signs, diagnosis, treatment

Thyroid hyperthyroidism - symptoms, signs, diagnosis, treatment of hyperthyroidism

Symptoms, signs, diagnosis, treatment of hyperthyroidism.





Hyperthyroidism is characterized by increased metabolism and increased levels of serum free thyroid hormones. There are many symptoms, but usually it is tachycardia, fatigue, weight loss and tremor. The diagnosis is made clinically and confirmed by laboratory tests. Treatment depends on the cause of thyrotoxicosis.


Hyperthyroidism can be established on the basis of the absorption of radioiodine by the thyroid gland, as well as on the basis of the presence or absence of circulating thyroid stimulants.


Etiology of hyperthyroidism



Hyperthyroidism can be the result of increased synthesis and secretion of thyroid hormones (T and T) by the thyroid gland, which is a consequence of the increased circulation in the blood of thyroid secretion stimulants or autonomous thyroid hyperfunction.It may also be the result of an increased release of thyroid hormones from the thyroid gland without increasing their synthesis. Such release is usually due to destructive changes in various types of thyroiditis. Hyperthyroid status can also be observed with various clinical syndromes.


Graves Disease(toxic diffuse goiter) - the most common A cause of hyperthyroidism, characterized by | Hyperthyroid state and one I or several of the following clinical features: goiter, exophthalmos and pretibial myxedema. These clinical manifestations are due to the formation of autoantibodies against thyroid TSH receptors; Unlike most autoantibodies that are inhibitors, these autoantibodies are stimulants that provide increased synthesis and secretion of excess T and T. Graves disease (as well as Hashimoto thyroiditis) is sometimes combined with other autoimmune pathologies, such as type 1 diabetes, vitiligo, premature graying of hair, perni-cyous anemia, connective tissue disease and polyglandular insufficiency syndrome.


Pathogenesis of infiltrative ophthalmopathy(and other lesions of the orbit - the cause of exophthalmos in Graves-Basedow disease) is not clear enough, but it is believed that this is the result of the action of immunoglobulins targeted at specific antigens in extraocular muscles and orbital fibroblasts. Ophthalmopathy can occur before the manifestation of hyperthyroidism or many years later (up to 20 years) after and often irrespective of the deterioration or improvement of the clinical course of hyperthyroidism. A typical ophthalmopathy with a constantly normal function of the thyroid gland is called eurythoid Graves' disease.


Violation of normal secretion of TSHis a rare reason. In patients with hyperthyroidism, the level of TSH can be undetectable, with the exception of cases with TSH-secreting adenoma of the anterior pituitary gland or pituitary resistance to thyroid hormone. The level of TSH is high, and the produced TSH for both diseases is biologically more active than normal TSH. An increase in a-subunit TSH in the blood (helps in differential diagnosis) occurs in patients with TSH-secreting pituitary adenoma.


Pregnancy large fruit, choriocarcinoma and hyperemesis (excessive vomiting) of pregnant women account for high levels of serum human chorionic gonadotropin (hCG), which is a weak stimulator of the secretion of thyroid hormones. The level of hCG is the highest in the first trimester of pregnancy, helps to reduce serum TSH and a slight increase in Tfreesometimes observed by this date. Increased thyroid stimulation may also be due to an increased level of partially desialized human chorionic gonadotropin (hCG), a type of hCG and a much more potent stimulator of thyroid hormone secretion than a more sialized hCG. Hyperthyroidism, which develops during pregnancy with a large fetus, with chorio-carcinoma and hyperemesis of pregnant women is short-lived; thyroid function is restored after generic resolution, appropriate treatment of choriocarcinoma, or at the termination of gi-remesis of pregnant women.


Non-autoimmune autosomal dominant hyperthyroidismmanifests in the period of early childhood. The condition is the result of a mutation in the TSH receptor gene responsible for the continuation of stimulation of thyroid hormone secretion.


Toxic solitary or multinodular goiter(Plummer’s disease) is the result of a mutation in the TSH receptor gene that provides thyroid stimulation. In patients with toxic goiter, autoimmune manifestations or circulating antibodies occurring in Graves' disease are not observed. In addition, in comparison with Graves' disease with toxic solitary and multinodular goiter, there is usually no remission.


Inflammatory diseases of the thyroid gland(thyroiditis) include subacute granulomatous thyroiditis, Hashimoto thyroiditis, asymptomatic lymphocytic thyroiditis, a variant of Hashimoto thyroiditis. Thyrotoxicosis can be the result of destructive changes in the thyroid gland and the release of hormones from the depot, but not an increase in the synthesis of hormones. Following this, hypothyroidism may occur. Irradiation of the organs of the neck in large doses in the treatment of malignant neoplasms of non-thyroid etiology, such as Hodgkin's lymphoma or laryngeal cancer, often leads to primary hypothyroidism.


Drug-induced hyperthyroidismmay occur with lithium therapy leading to goiter, with or without hyperthyroidism or hypothyroidism.Amiodarone and interferon a can induce thyroiditis with hyperthyroidism and other thyroid pathology. Patients receiving these drugs should be under close medical supervision.


Artificial (iatrogenic) thyrotoxicosisis a state of hyperthyroidism, which is a consequence of an accidental overdose of thyroid hormones.


Overdose of iodine preparationscauses hyperthyroidism and is characterized by low accumulation of radioiodine in the thyroid gland. Most often, this condition develops in patients with non-toxic nodular goiter (especially in the elderly) who receive drugs containing iodine (for example, amiodarone, iodine-containing expectorant drugs), or in patients who have undergone a X-ray study using radioiodine preparations. The etiology may include the formation, upon receipt of an excess of iodine, of a reserve of substrate for autonomous (not under the influence of TSH regulation) synthesis of thyroid hormones in certain sections of the thyroid tissue. Hyperthyroidism usually persists for as long as iodine continues in the bloodstream.


Metastatic Thyroid Canceris a possible cause of the development of this state. Hyperproduction of thyroid hormones is observed with functioning metastatic follicular carcinoma infrequently, but it happens, especially in the case of metastases to the lungs.


Ovarian goiter(struma ovarii) develops when the ovarian teratoma contains enough thyroid tissue, 4 liters, which leads to true hyperthyroidism. When | In this case, the accumulation of a radionuclide is observed in the pelvic region, and the accumulation of contrast by the thyroid gland is reduced.


Thyrotoxic Crisis- an acute form of hyperthyroidism, which is the result of untreated or poorly treated expressed hyperthyroidism. The condition develops quite rarely and occurs in patients with Graves' disease or a toxic multinodular goiter (solitary toxic node is less characteristic and usually not dangerous). The development of the condition can be triggered by infection, trauma, surgery, embolism, diabetic ketoacidosis, or toxicosis of pregnant women.


Pathophysiology of hyperthyroidism



With hyperthyroidism, the serum level of T increases more than T, possibly because of increased secretion of T and increased conversion of T to T in peripheral tissues.In some patients, only T is elevated (so-called T-toxicosis). T-toxicosis can also occur in other diseases associated with hyperthyroidism, including Graves' disease, multinodular goiter and an autonomously functioning solitary thyroid gland. If T3- do not treat toxoid goats, patients usually have changes in laboratory parameters characteristic of hyperthyroidism (an increase in T4and increased accumulation31). Various forms of thyroiditis, as a rule, have a hyperthyroid phase in their development and usually the next phase of hypothyroidism.


Symptoms and signs of thyroid hyperthyroidism



Most of the symptoms and signs are the same, regardless of the cause of the hyperthyroidism. The exceptions are infiltrative ophthalmopathy and dermopathy, which are found only in the case of Graves' disease.


Clinical manifestationscan be extremely pronounced or poorly perceptible. There may be a goiter or knot-formation. Most of the common signs and symptoms of hyperthyroidism are similar to adrenergic symptoms, such as nervousness and irritability, palpitations, hyperactivity, sweating,increased heart rate, fatigue, increased appetite, loss of body weight, insomnia, and frequent stools (sometimes diarrhea). Hypoma norea may be present. Symptoms may also include warm, moist skin, tremor, tachycardia, a large variation in pulse pressure, atrial fibrillation, and tachycardia.


Elderly patients, especially with toxic nodular goiter, may have atypical symptoms (apathetic or masked hyperthyroidism), more like depression or dementia. Most do not have exophthalmos or tremors. Symptoms such as atrial fibrillation, signs of impaired sensitivity, heart failure, and weakness are more common. And there may be clinical symptoms of damage only from one organ or system of organs.


Eye symptomsincludes an expressive look, lagging of the eyeball when looking to the side and a moderate injection of the conjunctiva, largely due to excessive adrenergic stimulation. Symptoms usually decrease with proper treatment.Infiltrative ophthalmopathy is more characteristic of Graves' disease, in which it reaches its maximum development and may occur years after the development of hyperthyroidism or several years before it. Ophthalmopathy is characterized by orbital pain syndrome, lacrimation, irritation (foreign body sensation), photophobia, hypertrophy of retrobulbar tissues, exophthalmos, and lymphocytic infiltration of extraorbital muscles, which causes lens muscle weakness, which often leads to diplopia.


Infiltrative dermopathy, also called pretibial myxedema (the term in this case is not entirely successful, as true myxedema is a manifestation of hypothyroidism), characterized by the absence of digital indentations, usually in the pretibial zone due to a kind of infiltration with a protein-like basic substance. Symptom is quite rare in Graves' disease, not associated with ophthalmopathy. In the early stages of development, damage to the skin is often accompanied by itching and erythema, as the skin develops a brownish tint.Infiltrative dermopathy may appear years after the development of hyperthyroidism or a few years before it.


Thyrotoxic Crisisdevelops suddenly and causes a whole bunch of symptoms, manifested alone or in combination; these are symptoms such as fever, marked weakness and muscle laxity, extreme anxiety with pronounced emotional arousal, confusion, psychosis, coma, nausea, vomiting, diarrhea and hepatomegaly with moderate jaundice. The patient may experience symptoms of cardiovascular collapse and shock. Thyrotoxic crisis is a life-threatening condition and requires urgent therapeutic interventions.


Diagnosis of thyroid hyperthyroidism



The diagnosis is based on anamnesis, physical examination of the patient and laboratory studies of thyroid function. Determination of serum TSH is the best method for verifying a diagnosis, since TSH secretion is inhibited in hyperthyroid patients, except in cases where TSH-secreting pituitary adenoma or pituitary resistance to thyroid hormones are present.At the same time, T can be normal in the case of true hyperthyroidism in patients with severe systemic diseases (similar to how a false low T level is recorded in the case of an euthyroid syndrome syndrome) and with T-toxicosis. If T is normal and TSH is low in a patient with mild clinical signs and symptoms of hyperthyroidism, serum T should be determined to confirm T-toxicosis; an elevated level confirms the diagnosis.


The cause of development is often established clinically (for example, an established history of medication, the presence of symptoms characteristic of Graves disease). If necessary, a scintigraphic examination using radioactive iodine preparations is prescribed.31. In cases when hyperthyroidism is caused by an increased synthesis of thyroid hormones, an increased accumulation of radioiodine with thyroid tissue is recorded.


Antibodies to the TSH receptor may be determined to verify the Graves-Bazedov disease, but this study is rarely used, except in the third trimester of pregnancy, to exclude the risk of developing Graves' disease of newborns.Antibodies to the TSH receptor easily overcome the placental barrier and stimulate the thyroid gland of the fetus. Most patients with Graves' disease have circulating antibodies to thyroid peroxidase and few patients - anti-thyoglobulin antibodies.


Primary violation of TSH secretion is not characteristic. The diagnosis is confirmed when hyperthyroidism occurs, with an increased circulating Tfreeand normal or elevated serum TSH.


If there is iatrogenic thyrotoxicosis caused by an overdose of thyroid hormones, there may be a need to determine serum thyroglobulin; it is usually reduced or normal, unlike all other causes of hyperthyroidism.


In cases where hyperthyroidism is caused by a random overdose of iodine preparations, a low level of accumulation of radioiodine by thyroid tissue is characteristic, because the accumulation of radioiodine by the thyroid gland is inversely proportional to the absorbed dose.


Treatment of thyroid hyperthyroidism



Treatment depends on the cause of hyperthyroidism.

Treatment with iodine preparations.Iodine in pharmacological doses inhibits the release of T and T for several hours and inhibits the organization of iodine, the transient effect persists from a few days to a week,after which the inhibitory effect is terminated. Iodine is used in emergency treatment to relieve a thyrotoxic crisis in patients with hyperthyroidism, in preparation for an emergency surgical procedure not related to the thyroid gland, and for preoperative preparation of patients with hyperthyroidism in the case of subtotal thyroidectomy (due to a decrease in thyroid vascularization). Iodine preparations are usually not used for the routine treatment of hyperthyroidism. The usual dose is 2-3 drops (100-150 mg) of a concentrated solution of potassium iodide 3-4 times a day or from 0.5 to 1 g of sodium iodide in 1 liter of 0.9% NaCI solution, administered intravenously, slowly over hours. .


Complications of iodine therapyare the development of inflammation of the salivary glands, conjunctivitis and skin rashes. Sodium ipodate and iopanoic acid replace excess iodine and support the inhibition of the conversion of T to T. The combination of one of these substances and dexamethasone also contributes to the inhibition of the conversion of T to T, can level the severity of symptoms of hyperthyroidism and restores the concentration of serum T to normal in about a week.


Therapy with propylthiouracil and methimazole. These thyreostatic drugs block the thyroid peroxidase, lower the iodine organization and disrupt the reaction of the paired compound (condensation). In high doses, propyl-oracil also inhibits the peripheral conversion of T to T. Twenty to 50% of patients with Graves disease develop remission after a 1-2 year course of treatment with drugs from these groups. Reducing the size (or returning to normal size) of the thyroid gland, restoring the normal level of serum TSH and reducing the clinical severity of hyperthyroidism before treatment is a good predictor of prolonged remission in the future. The combined use of thyreostatic therapy and the administration of L-thyroxine do not increase the length of the remission period in patients with Graves' disease. In toxic nodular goiter remission is rarely observed. Thyrostatic therapy is prescribed only for the period of preparation for surgical treatment or radioiodine therapy.


The usual starting dose of propylthiouracil is 100-150 mg per os after 8 hours and methimazole 5-20 mg 3 times a day.When the levels of T and T are normalized, the dose can be reduced to the minimum effective and is usually 50 mg 3 times a day or methimazole 5-15 mg once a day. Laboratory control, as a rule, is appointed in 2–3 months. Earlier control may be necessary to increase the dose of propylthiouracil to 150–200 mg every 8 hours. Such doses or higher (up to 400 mg every 8 hours) are usually prescribed to severe patients with thyrotoxic crises. Supportive therapy can last from a year to several years and depends on the clinical course of the disease. Car-bimazole, widely used in Europe, is quickly converted into methimazole in the body. The usual starting dose is the same as that of methimazole; maintenance dose is 5-20 mg 1 time / day. 2.5–10 mg 2 times / day or 1.7–6.7 mg 3 ra-day / day.


Side effects include the occurrence of allergic reactions, impaired liver function and (approximately 0.1% of patients) reversible agranulocytosis. Patients with allergic reactions to one drug may have reactions to another, although cross-sensitivity may also occur. If agranulocytosis develops,the patient cannot be treated with another drug; another method of therapy (for example, surgical treatment, radioiodine therapy) may well be used.


Each drug has its own indications and contraindications. Methimazole should be administered only once a day, which improves the compliance of therapy. In addition, when the dose of methimazole is less than 40 mg / day, agranulocytosis is less likely to occur. With propylthiouracil therapy, agranulocytosis can begin at any dose. Treatment with propylthiouracil is more preferable in cases where it is necessary to perform therapy with rheostatic drugs during pregnancy or breastfeeding, because this drug is less likely to overcome the placental or lactational barrier. However, methimazole was successfully applied in pregnant and lactating women, without causing any complications in the embryonic or neonatal period. Propylthiouracil is also preferable to prescribe for relief of thyrotoxic crisis, since the dose of the preparation used for this (800-00 mg / day) partially blocks the peripheral conversion of T.sub.T.


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