--> DISEASES OF TIROIDE

 

THYROID DISEASES   1

 

by dr Claudio Italiano

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Anatomy . The thyroid (t) is an endocrine gland ( internal secretion), which is located in anterior region of the neck, in front of the trachea, and it consists of 2 lateral lobes, united by an isthmus. The gland takes lateral relations with sternumcleidomastoideous muscle and the carotid, the laryngeal nerve, the trachea and the esophagus. His relationship with nerve is important for compression action on the nerve (dysphonia). The T. is vascularizated by two thyroid arteries, higher branches of the internal carotid artery. From the point of view anatomical microscopic, the functional unity is the "follicle", of about 300 microns in diameter, cubic form that surround the follicular cavity, filled with colloid substance, formed by the thyroglobulin, which includes iodinic thyrosinic residues and represents the deposit form of thyroid hormones.
 

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The thyroid hormones. They are formed by thyroxine, triiodothyronine and T4, T3. They consist of iodine for the 65% . The daily intake of iodine is therefore essential for the formation of hormones and varies from 20 to 600-1000 micrograms / day; in areas where iodine is insufficient many people are affected by hypothyroidism endemic goiter, due to the gland hyperhrophyertrofia to lack of iodine and by TSH stimulation.

The thyroid is, in fact, hungry for iodine and picks all available iodine (the trap of iodide), according to a pump mechanism to transport active energy-dependent. The uptake of iodine (I) depends by hipotalamic hormone, TSH, or hormone stimulation of the thyroid. The Iodine captured is, in turn, incorporated in thyrosinic radical of thyroglobulin, through a process of oxidation, catalysed by a perossidasic system. This stage is modulated by metabolic agents and is physiologically stimulated by TSH. The I. will be filed as well thyroxine or T4, with 4 molecules of iodine, or triiodothyronine or T3, incorporated in the thyroglobulin. Molecule.
The release of thyroid hormones, however, takes place through the proteolysis of thyroglobulin by protease and peptidases, by production of free T3 and T4. But T3 is the active hormone true. Two serum proteins, TbG or thyroid hormone-binding globulin and the TbPA, or " thiroid binding prealbumin "are necessary to transport. The main metabolic transformation of thyroid hormone is expressed through consecutive removals of individual atoms (monodeiodinetions), which ultimately lead to total loss of iodine content in the organic molecule.
Mechanisms for monitoring thyroid function. The regulation of the T. is aimed at maintaining adequate levels of circulating T3 and T4 and is entrusted to 3 control systems: the first is the release of pituitary TSH, thyroid stimulating hormone, (in turn controlled by a feed back mechanism , by TRH, "thyrotropin releasing hormone), the second intrathyroid consists in the possibility of the self-liberation of T3 and T4, depending on the levels of intracellular organic iodine, and the third, perferic one, is represented by the microsomal and monodeiodinase the consequent transformation of T4 into T3, the more biologically active.
Biological effects of the consumption of thyroid hormones. The action longest known is the increase of oxygen consumption and production of heat. These effects depend by activation of cellular respiration and metabolism due to T3 and T4. Metabolic thyroid hormones stimulate glycogenolysis, by production of hyperglycaemia and action on neoglycogenesiys. On lipid metabolism they have a lipolytic action, through the activity of catecholamines. Finally at low doses have protidoanabolic action. The heart is the T4 and T3 trigger, by tachycardiac action and increase pump; on the digestive tract, is determinated an increased of motility but a reduction of absorption. On the skeletal system, the action will be activation of osteoclasts and, therefore, bone resorption. Direct action on mitochondria (power cell) determine an increase ATP production and consumption of oxygen. It would seem, therefore, that the thyroid hormones rather than a single site of action have multiple locations and coordinated control handle.
Investigations to evaluate the effects of hormones. Calculation of basal metabolic rate based on the feedback of oxygen consumption patient fasting, expressed as the percentage change compared to normal. The speed of contraction and release muscle was apparently used in the diagnosis of syndromes of hyper or hypothyroidism. The detection of low cholesterol and increased calcium in found in the hyperthyroidism and, conversely, a decrease in cholesterol in the hypothyroidism.

Investigations directed. The measurement of thyroid uptake of radioiodine is one of the most frequently used techniques. It is the determination of incorporation of a radiocompound in the thyroid, after some time, usually at 6 ° and 24 ° hours, and it is between 5-25% of the administered dose. If the thyroid gland has decreased activity, catchment will be diminished, while in hyperthyroidism it will be increased.
 
The thyroid scintigraphy, however, is a survey to assess the distribution of a radioactive dye IODATE (radioiodine) in the parenchyma of the thyroid, so that areas hypercoloured are signed by a computer, and take conventional staining yellow and red (bright colours) and areas hypocoloured in blue and green, so you can distinguish the cold nodules, hypocaptanti, or suspected displasic or neoplastic areas (in fact the tumour tissue loses its collection function) and hot nodules, or furnishings hypercoloured (thyroid adenoma, m. plummer, toxic adenoma).
Finally you can dose thyroid hormones, which are largely, however, linked to TbG and TbPA. The direct dosage is possible, by radioimmunological methods and gives the values of free hormone, which is the most metabolic active, and therefore fT3 and fT4. The radioimmunological determination of TSH takes also considerable significance so that
it allows us to assess whether the gland is stimulated or not, the values are between 0.5 and 5.0 microUnità / ml, for example in hypothyroidism, due to primary gland insufficiency, TSH levels are consistently high, while in primary forms with hyperthyroidism, for example in toxic Adenoma of Plummer, the TSH level will be zero (tireotossicosys).

The test to TRH, on the other hand, will assess the reserve of pituitary hormone TRH, which is limited also in hypothyroidism due to hypothalamus-pituitary insufficiency. The test takes advantage of the administration of TRH which increases in normal individuals whose TSH values are between 5 and 20 microUnità / ml. The answer is exalted in the hypothyroid subject. Other investigations are antibodies finding and anti anti-thyroglobulin anti anti-thyroid- microsomes in the event of Hashimoto thyroiditis and in a considerable number of subjects with Basedow's disease and hypothyroidism and immunoglobulin tireostimolanti (IST), typical of Basedow.

PATOLOGICAL CONDITIONS RELATED TO INCREASE AND REDUCTION OF THYROID HORMONES

Whenever the availability of thyroid hormone is excessive respect to the physiological need of tissue, this clinic condition is called hyperthyroidism. The most common forms are represented by toxic goiter or Graves’ disease, and Flajani Basedow, (MdB), which is characterized by a diffuse goiter, signs of thyrotoxicoses and cellular infiltration of mucopolysaccharides with protrusion of the eye and bulbs, ophthalmopathia and infiltration dermatitis. This clinical condition affects the female (7:1) and haplotypes associated with HLA-B8, Drw3, BW 35 and BW 46. In the same families increased incidence appears to be due to an alleged autoimmune origin, for example associated with other autoimmune diseases (whose genesis depends on a movement of antibodies against the same structures of his body).
 


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