Thyroid diseases are both functional and morphological. However, to understand thyroid pathology it is necessary to know some of the known thyroid secretion products known to date: thyroid hormones triiodothyronine (T3) thyroxine (T4) and calcitonin. Iodine capture is by a mechanism involving a special conveying protein called simporter (transporting iodine and sodium simultaneously); . Both iodine oxidation and thyroglobulin synthesis and the introduction of iodine into the protein structure are made by an enzyme called thyrotoperoxidase. The process is controlled by the pituitary by a feed-back mechanism via TSH that stimulates the morphological growth and function of thyroid cells, the increase in the thyroid size and its vasculature. The feedback mechanism between TSH and thyroid hormones results in: when the thyroid makes more thyroid hormones, they also sign up to the pituitary and cause a decrease in TSH.
In the mirror, when the thyroid does not produce enough thyroid hormones, there is an increase in TSH, an increase in the thyroid size and its secretion. It is noteworthy that there is a period of weeks between the change in thyroid hormone concentration and the alteration of TSH, At the cardiovascular level, catecholamines are receptive to specific receptors and modulates the excitability, conductivity and contractility of the heart. It also modifies the response of different hormones involved in vascular tone and maintaining blood pressure. At the digestive level it participates in the maintenance of digestive tract motility. The muscular effects are both metabolic and excitatory, Here are, in the opinion of the specialist, the conditions that can affect your thyroid! .
The common clinical picture of excess thyroid hormone is symptomatically characterized by involuntary weight loss, agitation, The skin is warm and wet, there is a fine tremor of the extremities, the muscle mass is diminished, the pulse is increased and the tension values are high, there is a characteristic increase in the difference between systolic and diastolic TA. Thyroid in many cases Paraclinic, in all cases of thyrotoxicosis, laboratory tests generally show elevated thyroid hormone levels. Ultrasound has a different appearance depending on the etiology of thyrotoxicosis. Sometimes, other imaging methods are used: thyroid scintigraphy, pituitary imaging. There are several causes of thyrotoxicosis: subacute thyroiditis, Basedow-Graves disease, hyperthyroidism, hyperthyroidism, Plummer adenoma, induced beta-induced thyrotoxicosis, iodine induced thyrotoxicosis, TSH secretory pituitary adenoma, thyroid hormone resistance, thyrotoxicosis faction and other rare forms of thyrotoxicosis .
Subacute thyroiditis is characterized by an inflammation of the thyroid in the context of a previous respiratory virus; . The characteristic is the general altered state, the high fever, embarrassing that goes to living pain, anterior cervical, with irradiation to the ears, accentuated by swallowing and palpation plus the signs of excess thyroid hormone mentioned in the general presentation of thyrotoxicosis. The thyroid is enlarged in volume and sensitive to palpation. From a paraclinical point of view, in addition to suppressed TSH and elevated thyroid hormone levels, inflammatory syndrome (leukocytosis, elevated VSH, CRP). Thyroid ultrasound shows an intense hypoecogenic, non-homogeneous pattern of thyroid parenchyma - sometimes only parcel, altadata of the entire thioid parenchymal - with a typical decrease in thyroid vasculature.
Scintigraphy is useful in the differential diagnosis of excess hormones. Treatment is nonsteroidal anti-inflammatory; . To improve the symptoms of thyrotoxicosis, beta blockers (pulse and high tension values), anxiolytic and hypnotic need are used during thyrotoxicosis. Following the follicular rupture phase hypothyroidism - generally transient - may sometimes require substitution treatment. Rarely, following subacute thyroiditis, especially if episodes are repeated, hypothyroidism may be required requiring unlimited treatment.
Basedow-Graves Disease is a hyperthyroidism produced by the secretion of aberrant autoantibodies: TRABs (produced in lymphocytes) that mimic TSH structural and increase thyroid size and function. Concomitantly with TRAB production, autoantibodies are produced against some structural thyroid proteins: thyroglobulin and thyrooperoxidase: ATPO and ATG. Disease is three times more common in women than in men, and may be associated with other autoimmune diseases. Clinically, the patient presents the common symptom of excess thyroid hormone to which either unilateral or bilateral exophthalmia (prominence of the eyeball outside the orbit) and rare skin lesion. Exoftalmia is caused by inflammation of the extrinsic muscles of the eyeball and can begin with or with thyroid disease.
It is more common in smokers. It may have wavy development, sometimes independent of hyperthyroidism. Paraclinically, the patient has suppressed TSH and elevated T3 and T4 levels; . The treatment is that of the hyperproduction of thyroid hormones and that of tyreotoxicosis. Synthetic antithyroid (Thiamazole) reduces the formation of thyroid hormones by inhibiting thyrotoperoxidase.
For symptomatic treatment, beta blockers and other associated antihypertensive agents are used. If needed anxiolytic and hypnotic. There are studies showing the utility of selenium supplementation. ATS treatment starts at high doses that decrease as thyroid hormone production decreases. It lasts for at least 6 months.
It is remarkable that the effects of tatament occur after at least 10-14 days after its initiation. Initially, the patient is monitored at 6 to 8 weeks. After balancing thyroid function, evaluations are rarer. If the patient wishes to become pregnant, if the disease is relapsed, it is necessary for a long period of time not to stop the medication. If adverse effects of synthetic anti-thyroid drugs occur or if there are suspected associated nodules, thyroididectomy and subsequent substitution with thyroid thyroid synthase.
In cases where the thyroid has low dimensions and there are no nodules, or if surgery is not accepted or if there is increased risk, radiotherapy. Ophthalmopathy benefits from hygiene, selenium supplementation, but may also require corticoid. In cases of opthalmopathy with no activity and motility disorders or if there is an ophthalmic nerve injury, surgical correction may be indicated. Multinodular hyperthyroidism is another common etiology of thyrotoxicosis. In this case, on the background of an old multinodular goiter, one or more nodules undergo TSH receptor activating mutations and become autonomous hysesecrets.
Symptomatology and clinical signs are the same as for other types of tootoxicosis. Paraclinically, TSH is suppressed with high levels of thyroid hormones. Thyroid ultrasound shows nodules with increased vasculature and scintigraphy shows hot nodules. After initiating antithyroid therapy and balancing thyroid function, surgical intervention is preferred. If this is risky or not accepted by the patient, medication may be used, noting that antithyroid drugs do not stop the growth of nodules and the occurrence of possible compression phenomena.
The Plummer adenoma is a hypersecreting node of thyroid hormones derived from a cell that undergoes a mutation. The adenoma grows and reaches a critical cell volume that causes TSH independent hormone hypersecretion and TSH suppression resulting in a diminution in the size of the remaining thyroid parenchyma. Symptomatology and laboratory clinical signs are similar to hyperthyroidism. Characteristic in scintigraphy is the appearance of the hypercaptant node with the lack of capture in the rest of the thyroid parenchyma. The treatment is initially performed with antithyroid drugs, with preference being given to surgery or radioiodine therapy.
Induced hyperthyroidism betahCG is determined by beta-hCG which, in some cases, has the same structure as TSH. Characteristically, hCG binds to the TSH receptor and increases thyroid size and function. The clinical picture overlaps with that of disgrace and is sometimes deceptive; . In pregnant women with thyrotoxicosis the first trimester disgration is more frequent and noisy. Paraclinic, elevated thyroid homologues are observed in the first trimester of the sacrifice, and then, with decreasing beta hCG values, the spontaneous remission of hyperthyroidism.
Generally, it does not require antithyroid treatment, but there are exceptional cases requiring low antithyroid doses over short periods of time. Since there is susceptible genetics for this thyrotoxicosis disorder, induced beta hCG will be repeated at all pregnancies. Induced iodine thyrotoxicosis is a condition resulting from exposure of the patient to exogenous exogenous iodine intake by supplements (spirulina, other seaweed, erythrozine) or drugs (a contrast substance used for tomography, urography, coronary artery or hysterosalpingography. Administration of iodine in amounts over the recommended daily dose is tolerated by most people without developing hypo or hyperthyroidism. However, there are people who, after exposure to large quantities of iodine, hyperthyroidism, especially if they come from a zone with iodine deficiency or have a pre-existing thyroid disorder: a multinodular chicken or autoimmune thyroiditis.
Hyperthyroidism may develop immediately after exposure to iodine or weeks and even months after exposure. The clinical and paraclinical picture is that of tyreotoxicosis. In half of the cases, thyrotoxicosis can occur spontaneously or is followed by a hypothyroid phase. Hyperthyroid therapy with antithyroid synthesis is preferred, given the negative effects of excess thyroid hormones on various systems, especially cardiovascular. If hyperthyroidism has occurred on a pre-existing gouty, surgery is preferred.
Source : csid.ro
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