Download Thyroid: thyroid hormone synthesis, biological effects. Endemic

Thyroid: thyroid hormone synthesis, biological effects. Endemic goiter.
Anatomy and physiology of the thyroid gland
The thyroid gland is the largest endocrine gland of the human body, which has only endocrine function.
Its weight in the adult average of 20g. The name is derived from the thyroid gland thyroid cartilage
adjacent larynx.
Front thyroid covered pretrahealnoy neck fascia plate that forms a fibrous capsule gland and fixes it to
the trachea and larynx muscles and skin. Of the fibrous capsule into the gland depart thin layer
separating the gland into lobules. Lobules are composed of follicles, whose walls are lined with cuboidal
epithelium. In a state of increased features follicular cells become cylindrical in hypofunction flattened.
The cavity is filled follicles homogeneous viscous yellowish colloid - a product of the epithelial cells of
follicles colloid consists mainly of thyroglobulin is iodinated glycoprotein with a molecular weight of
about 7000 000 etc. Consisting yodtirozinovye (mono - diiodotyrosine) iodothyronine (mono-, di-,
trpyodtironiny and thyroxine) and almost all the amino acids contained in the body. Found that 95% of
iodine found in the body is in the colloid.
Parafolikulyarno singly, in groups, in the thickness interfolikulyarnogo islet cells are light, closely
adjacent to the walls of capillaries and are called K-cells. The product of these cells is calcitonin - have
the ability to reduce the level of Ca 2 ^ levels by including it in the bones.
Product of the endocrine activity of the thyroid gland are iodinated hormones (T4 and then not
iodinated hormone calcitonin. Structural and functional unit of the thyroid gland is the follicle, the walls
of which are composed of thyrocytes. Synthesis of thyroglobulin and thyroid hormones are tireoitsitami.
Thyroid hormone biosynthesis occurs in 4 stages.
Stage I - the inclusion of iodine in the thyroid gland. Iodine in the form of organic and inorganic
compounds from food and water in the gastrointestinal tract and is absorbed in the intestine in the form
of iodide. Iodides of blood delivered to the thyroid gland, which is due to the action of active transport
and Na "- Cg - A I F - basics in the basement membrane tireoitsitov thumb Iodides at 2 mg per hour and
concentrate them.
Stage II - the conversion into molecular iodine. This stage is done by the enzyme peroxidase and 1
Whom as an electron acceptor. Peroxidase is directly related to the membrane thyrocytes.
Stage III - iodine organification D binds to a molecule tyrosine contained in thyroglobulin. When binding
of iodine with one molecule tyrosine formed MIT, two DIT.
Stage IV - oxidative condensation under the influence of oxidative enzymes from two molecules of DIT +
DIT = T4, DIT + MIT = T3. Biologically active are the only L-form (L-isomers) of thyroid hormones. The
process of formation of T4 and T 'is a molecule in tireotsite thyroglobulin, then T | II 1', move into the
lumen of the follicle, where they accumulate. Amount of thyroid hormones such nude them enough to
maintain the state of euthyroidism than a month.
Secretion of thyroid hormones in the blood is influenced by TSH. When the level of thyroid hormones in
the blood increases the secretion of TSH adenohypophysis. The latter binds to receptors on the thyroid
gland, activates adenyl cyclase, resulting in an increasing number of cAMP activates transport
thyroglobulin (contained in it T4 and T,,) from the lumen of the follicle to the lysosomes thyrocytes.
where, under the influence of proteolytic enzymes by proteolysis of thyroglobulin releasing T4 and T3,
diffusing from the lumen of the blood thyrocytes. Received the blood T4 and T3 binds to proteins
carrying out the transportation function. TSH binds 75% T4 and 85% T3, and T4 binds more tightly. In
addition, hormones bind to prealbumin thyroxine (it binds T4 and 15% less than 5% T,,), and about 10%
T4 and 10% T3 binds to albumin.
Thus, in the free form in the blood circulate only 0.03% of T4 and T3 0.3% It is a free form makes
biological effect.
T4 - is now seen as a prohormone of biologically active hormone T3. Within days synthesized 80-100
mcg of T4.
T3 - the biologically active hormone, a day it produces about 20-30 mg, with about 20% of this amount
(6-4 mg) is synthesized in the thyroid gland, and 80% (ie, 16-24 mg) is formed by conversion of T4 to T3
by the enzymes T4 - 51 - deyodinazy the periphery (mainly in the liver, kidney, pituitary gland).
The function of the thyroid gland (TG) and the adenohypophysis is as under mutual control, and under
the control of the supreme regulator of the neuroendocrine system - the hypothalamus. Major regulator
of the secretion of TRH and its transport to the pituitary gland is the monoaminergic neurons of the
hypothalamus and brain stem. Suppose! That noradrenergic system stimulates the production of TRH
and serotonergic - brakes. Maximum secretion observed in the morning and the minimum at midnight.
TRH inhibits secretion of hypothalamic somatostatin, which also inhibits the production of TSH. The
relative balance between the pituitary and the thyroid gland is done on a "plus-minus" interaction tropic
hormones of the pituitary and endocrine effector. Increased production of TSH leads not only to
enhance the biosynthesis of iodine-containing hormones, but also to diffuse or nodular hyperplasia of
the thyroid gland.
The biological action of thyroid hormones. Thyroid hormones have a complex multi-faceted impact on
all parts of the body, for all kinds of metabolism. They stimulate thermogenesis, enhance oxidative
processes, increase the absorption of O2 tissues, causing uncoupling of oxidative phosphorylation in the
mitochondria.
Fetal and neonatal thyroid hormones are essential for the morphological and functional development of
the brain and the body in general. Their failure in this period, leading to a rare anatomical and
neurological damage (until the development of cretinism).
Iodothyronine mother cross the placenta only in limited quantities, so the normal growth and
development of the fetus in utero depends mainly on its own hormones. In the mature organism to the
fore the metabolic effects of thyroid hormone, the principal of which are calorie-gene effect.
The main effects of thyroid hormones.
ensure the formation of the nervous system and the skeleton in the perinatal period;
increased O2 consumption in all tissues except the brain, spleen and testicles;
increase the production of heat;
have positive chronotropic and inotropic effects on the myocardium;
receptor sensitivity to catecholamines;
increases the number of catecholamine receptors in the heart muscle
regulate the activity of the respiratory center;
stimulate erythropoiesis;
accelerate the metabolism and clearance of hormones and drugs, leading to a compensatory increase in
the rate of their production;
stimulate both the formation and resorption of bone;
Action at the molecular level
T3 and T4 is associated with specific nuclear receptors linked to chromatin-tion
stimulate protein synthesis
affect cell membranes, changing the activity of Na-K-ATPase, which increases the intracellular transport
of glucose and amino acids.
Methods of investigation of patients with thyroid cancer.
I. Physical methods.
Clinical diagnosis of thyroid disease involves the identification of the patient symptoms of
hyperthyroidism, hypothyroidism, as well as changes in the structure of the thyroid gland.
In the diagnosis of diseases of the thyroid gland is a key place of her own palpation technique and ability
to interpret the results. During palpation of the prostate observed mobility, its consistency, the presence
or absence of its thicker sections seals (nodes), the degree of increase in cancer. T \ march various
classifications to assess the degree of enlargement of the thyroid gland. Classification of goitre (WHO,
1994)
0 no Zoba
1 - The size of the large values of the distal phalanx of the big
finger. Goiter palpable, but not visible.
II Goiter palpable and visible to the eye.
Iodine deficiency diseases. Endemic goiter.
Ioddefitsitnye diseases are one of the most common non-infectious human diseases. In general, on the
ground in regions with iodine in the environment inhabited 1.5 billion people, 655 million of them have
an enlarged thyroid gland (goiter according to WHO (1993). While the 40 million - severe mental
retardation due to iodine failure.
One of the major diseases of Iodine deficiency is endemic goiter.
Goiter - an enlarged thyroid gland develops as a result of iodine deficiency in people living in certain
geographical areas with iodine in the environment (ie, endemic goiter area).
Goiter. develops in people living outside endemic areas, called sporadic goiter. nude found in
mountainous (Alps, Altai, the Himalayas, the Caucasus, the Carpathians, the Tien-Shan, etc.), and the
plains (tropical Africa, South America, Western Ukraine, Belarus, Central Asia, Baikal, the Caucasus, the
Far East, etc. etc.), an area considered to be endemic, if 10% of the population have symptoms of goiter.
Women suffer more.
Etiology. The main reason - it's the lack of iodine in the body (iodine deficiency). Iodine - a trace mineral
that is required for the biosynthesis of thyroid hormones - T4 and T3. 90% of the daily requirement of
iodine is provided by food, 5.4% - water, about 4-5% comes from the air. When reducing the intake of
iodine than the daily need, develops a compensatory enlargement of the thyroid gland, ie. goiter. If
normal daily nutrient requirement of iodine is 200-250 mg / day, in endemic goiter area in the body
receives less than 50 mg / day.
Factors predisposing to the development of endemic goiter:
family history, family history of goiter
Genetic defects in the biosynthesis of thyroid hormones
urohromom water pollution, nitrates, high content of Ca ", humic substances, which impairs absorption
of iodine.
shortage in food and in the environment of trace elements: zinc, manganese, selenium, molybdenum,
cobalt, copper and excess Ca + +. Imbalance of trace elements contribute to disruption of the
biosynthesis of thyroid hormones
drugs that block the transport of iodine in the thyroid cells (periodate, potassium perchlorate)
the use of drugs that violate the organification of iodine in the thyroid gland (thiourea derivatives,
propiluratsila some sulfonamides, aminosalicylic acid)
goitrogen presence in foods. Goitrogen: thiocyanate contained in cabbage, turnips, lettuce, horseradish,
corn, Ma NIOC, sweet potatoes, beans and other Roman
impact of infectious inflammatory processes, especially chronic, parasitic infestations, satisfactory
sanitation and social conditions.
Pathogenesis. Given the lack of iodine is reduced synthesis of thyroid hormones, which leads to
secretion of TSH nkshvatsip also increases the sensitivity of thyrocytes to stimulating effect of TSH.
Gender influence TSH is hypertrophy and hyperplasia in the future and thyrocytes. When TSH
stimulation of the thyroid gland is a compensatory intensification of the absorption of iodine and other
stages ipgratireoidnogo metabolism. One of the manifestations of adaptation is the increased
production of T3, the synthesis of which requires at 4, and 3 atoms of iodine. Sometimes, due to
imperfections in the compensatory mechanisms hyperplasia thyrocites individual can acquire the
properties of autonomy or neoplasia (uncontrolled cell division and growth).
A reflection of adaptive mechanisms, developing in endemic goiter, is also increasing education T3 from
T4.
In the development of goiter is the insufficient synthesis of thyroglobulin in the endemic areas, which
leads to poor education T4.
According to modern concepts, autoimmune factors play a large role in the development of endemic
goiter.
Classification.
1. The degree of swelling of the thyroid gland (goiter size) according to the WHO (0. I, II):
a. Histological b. Colloidal c. Parenchymal.
2. In the form:
a. Diffuse b. Nodal c. Mixed.
3. By function:
a. Euthyroid b. Hypothyroid
4. Localization:
a. Usually located b. Partly retrosternal;
a. Ring, was dystopic crop of embryonic-tion bookmarks (goiter tongue, extra thyroid lobe).
Classification of goiter by the WHO (1994). Oh, no crop
I - Dimensions share more of the distal phalanx of the thumb. Goiter palpable, but not visible.
II - Goiter palpable and visible to the eye. Criteria of severity of endemic goiter
Since 1992. in assessing the severity of endemic goiter uses standardized criteria recommended by the
WHO and the International Committee for the control of iodine deficiency disorders. They are presented
in the table.
Table № 1
Criterion Group severity of iodine deficiency diseases
Light Medium Heavy
The incidence of goiter% (according to ultrasound) Students 20-29,9 5-19> 30
The number of listening goiter (palpation) Students 5-19 20-29.9> 30
Median urinary iodine mg / 'l Students 50-99 20-49 <20
The number of divisions with the level of TM-5mMG / d% newborn-degenerate 3-19.9 20-39.9> 4 ()
Median gireogdobudina. ng / ml of Children, Adults
Table number 2. Norms of daily iodine intake (WHO, 1996).
Of the population norm of daily consumption
Infants (first 12 months) 50
Children (2 to 6 lay) young children 90
School-age children (7-12 years) 120
Adult (1 2> 4 above) 150
Variables and lactating women 200
Clinic. Clinic goitre determined by the degree increases, the form and function of the thyroid gland. Even
with the euthyroid state, patients may complain of general weakness, fatigue, headache, discomfort in
the heart area. Usually these complaints appear at high magnification and reflect functional disorders of
the nervous and cardiovascular systems. As the compression of adjacent organs there are complaints at
the World Cup. "SEC) pressure in the neck, which is increasing in the supine position, the difficulty in
breathing and swallowing. occasional bouts of breathlessness, dry cough. Palpable thyroid gland is
enlarged, homogeneous, soft-| dns111chnoy consistency, sometimes indicated moderate density.
Prevention and treatment. There are: - Mass: - Group: - individual prevention.
I. Mass is achieved by the addition of iodine (iodide or potassium iodate) in the most common foods:
salt, bread, water. In Russia, the standard adopted for iodized table salt - 40 ± 15 mg of iodine per 1 kg
of salt n saw yolata potassium. Between prevention and treatment of endemic goitre there is no
fundamental difference, therefore, treatment of endemic goitre involve assigning the appropriate doses
of iodine yoda.Protivopokazaniya the appointment is:
- Thyrotoxicosis of any etiology;
nodular goiter (hot site) or at lower basal TSH concentrations less than 0.5 mIU / liter.
II. The group held antistrumin prevention (Table 1. - 1000 mcg of iodine) 0.001 g of potassium iodide.
Potassium iodide -100.
III.
Treatment.
References:
1. Balabolkin MI Endocrinology, Moscow, 1998
2. Vladimir Potemkin Endocrinology, Moscow, 1999.
3. Grandparents II Endocrinology, Moscow, 2000.
4. G.A.Melnichenko, O.V.Udovichenko, A.E.Shvedova. Endocrinology. Typical errors practitioner-2012.
frequent errors in diagnosis and treatment of diseases of the endocrine system. Separate chapters are
devoted to diseases of pituitary, thyroid, parathyroid, obesity, osteoporosis, etc.
5. S.B.Shustov, Yu S. Khalimov GE Trufanov functional and topical diagnosis in endocrinology, 2010.
6. GA Melnichenko A.Yu.Tokmakova, D.E.Koloda, N.V.Lavrischeva. Endocrine disease. 2009 Guidelines
for Pediatric Endocrinology. Handbook of Clinical Pediatric Endocrinology Edited by Charles GD Brook,
Rosalind S. Brown. 2009.
7. D. Gardner, D. Shobek. Basic and clinical endocrinology. Book 1. Greenspan's Basic & Clinical
Endocrinology. 2010.
8. D.Gardner, D.Shobek. Basic and clinical endocrinology. Book 2. Greenspan's Basic & Clinical
Endocrinology. 2011.
9. Clinical Endocrinology. Edited by EA Kholodova. 2011.
10. Endocrinology. National guidelines (+ CD-ROM). 2012. National guidelines - a series of practical
guides for major medical specialties, including specific information needed for continuous medical
postgraduate obrazovaniya.god.
More:
1. Edited by EA Kholodova Handbook of Clinical Endocrinology. Minsk. Belarus, 1996.
2. Therapeutic Handbook (Washington, translated from English), 1996 (section endocrinology).
3. Edited by Starkova NT, Manual of Endocrinology, Medicine, 1996
4. Edited by H. Lavin, Endocrinology. Practice. Moscow, 1999.
5. Endocrinology. Diabetes. Fadeev PA A Reference Guide. 2009.
6. I.B.Manuhin, L.G.Tumilovich, M.A.Gevorkyan. Gynecological endocrinology in 2012. lectures on
gynecological endocrinology.
7. A.V.Kartelishev, Alexander Rumyantsev, N.S.Smirnova Actual problems of obesity in children and
adolescents. 2010.
8. AN ham. Emergency Endocrinology. 2011. diagnosis and treatment of emergency conditions
associated with endocrine diseases, outlines coma in patients with diabetes mellitus.
9. A.M.Mkrtumyan, A.A.Nelaeva. Emergency Endocrinology. 2010.
10. N. A.Petunina, L.V.Truhina. Thyroid disease. 2011.
11. G.M.Kronenberg, Sh.Melmed, K.S.Polonski, P.R.Larsen. Thyroid disease. Williams Textbook of
Endocrinology. 2010.
12. G.M.Kronenberg, Sh.Melmed, K.S.Polonski, P.R.Larsen. Diseases of the adrenal cortex and endocrine
hypertension. Williams Textbook of Endorcinology, 11th edition. 2010.
13. Treatment of diseases of the thyroid gland by traditional and non-traditional ways. 2010.
Internet sites:
1. "Internet Portal: HINARI»; 2. medscape.com; 3. Alltheweb.com; 4. Yahoo.com.
5. E-medicine.com.