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ЭБС "КОНСУЛЬТАНТ СТУДЕНТА"
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-read table-responsive">="t"pan class="">ANATOMY OF THE THYROID GLANDn class="">ANATOMY OF THE THYROID GLANDclass="">ANATOMY OF THE THYROID GLAND>ANATOMY OF THE THYROID GLANDNATOMY OF THE THYROID GLANDTOMY OF THE THYROID GLANDY OF THE THYROID GLANDOF THE THYROID GLAND THE THYROID GLAND

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Increase of oxygen absorption by cells with the activation of oxidative processes and increase of basal metabolism.

Stimulation of protein synthesis by increasing the permeability of cell membranes for amino acids and activation of cell genetic apparatus.

Improving the efficiency of the mitochondria and myocardial contractility.

Regulation of heat generation and heat transfer.

Increase of excitability of the central nervous system and activation of mental processes.

The protective effect against the stress myocardial damage and ulceration.

Increase of renal blood flow, glomerular filtration and urine output.

Support for sexual and reproductive functions.

Participation in the regulation of calcium levels in the blood.

pan class="">Increase of oxygen absorption by cells with the activation of oxidative processes and increase of basal metabolism.

Stimulation of protein synthesis by increasing the permeability of cell membranes for amino acids and activation of cell genetic apparatus.

Improving the efficiency of the mitochondria and myocardial contractility.

Regulation of heat generation and heat transfer.

Increase of excitability of the central nervous system and activation of mental processes.

The protective effect against the stress myocardial damage and ulceration.

Increase of renal blood flow, glomerular filtration and urine output.

Support for sexual and reproductive functions.

Participation in the regulation of calcium levels in the blood.

n class="">Increase of oxygen absorption by cells with the activation of oxidative processes and increase of basal metabolism.

Stimulation of protein synthesis by increasing the permeability of cell membranes for amino acids and activation of cell genetic apparatus.

Improving the efficiency of the mitochondria and myocardial contractility.

Regulation of heat generation and heat transfer.

Increase of excitability of the central nervous system and activation of mental processes.

The protective effect against the stress myocardial damage and ulceration.

Increase of renal blood flow, glomerular filtration and urine output.

Support for sexual and reproductive functions.

Participation in the regulation of calcium levels in the blood.

class="">Increase of oxygen absorption by cells with the activation of oxidative processes and increase of basal metabolism.

Stimulation of protein synthesis by increasing the permeability of cell membranes for amino acids and activation of cell genetic apparatus.

Improving the efficiency of the mitochondria and myocardial contractility.

Regulation of heat generation and heat transfer.

Increase of excitability of the central nervous system and activation of mental processes.

The protective effect against the stress myocardial damage and ulceration.

Increase of renal blood flow, glomerular filtration and urine output.

Support for sexual and reproductive functions.

Participation in the regulation of calcium levels in the blood.

s="">Increase of oxygen absorption by cells with the activation of oxidative processes and increase of basal metabolism.

Stimulation of protein synthesis by increasing the permeability of cell membranes for amino acids and activation of cell genetic apparatus.

Improving the efficiency of the mitochondria and myocardial contractility.

Regulation of heat generation and heat transfer.

Increase of excitability of the central nervous system and activation of mental processes.

The protective effect against the stress myocardial damage and ulceration.

Increase of renal blood flow, glomerular filtration and urine output.

Support for sexual and reproductive functions.

Participation in the regulation of calcium levels in the blood.

"">Increase of oxygen absorption by cells with the activation of oxidative processes and increase of basal metabolism.

Stimulation of protein synthesis by increasing the permeability of cell membranes for amino acids and activation of cell genetic apparatus.

Improving the efficiency of the mitochondria and myocardial contractility.

Regulation of heat generation and heat transfer.

Increase of excitability of the central nervous system and activation of mental processes.

The protective effect against the stress myocardial damage and ulceration.

Increase of renal blood flow, glomerular filtration and urine output.

Support for sexual and reproductive functions.

Participation in the regulation of calcium levels in the blood.

>Increase of oxygen absorption by cells with the activation of oxidative processes and increase of basal metabolism.

Stimulation of protein synthesis by increasing the permeability of cell membranes for amino acids and activation of cell genetic apparatus.

Improving the efficiency of the mitochondria and myocardial contractility.

Regulation of heat generation and heat transfer.

Increase of excitability of the central nervous system and activation of mental processes.

The protective effect against the stress myocardial damage and ulceration.

Increase of renal blood flow, glomerular filtration and urine output.

Support for sexual and reproductive functions.

Participation in the regulation of calcium levels in the blood.

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onClick="{{;;call_submit('frm_rds','rds','rds|rds','popup_image(doc,ISBN9785970439272-0008,POPUP-Xz17-pic_0168.png,911,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">ie=yes" asis-dx="2025" asis-dy="1931" popup="POPUP-Xz17-pic_0168.png;911;868" onClick="{{;;call_submit('frm_rds','rds','rds|rds','popup_image(doc,ISBN9785970439272-0008,POPUP-Xz17-pic_0168.png,911,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">z17-pic_0168.png,911,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">7-pic_0168.png,911,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">pic_0168.png,911,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">c_0168.png,911,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">0168.png,911,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">68.png,911,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">.png,911,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">ng,911,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">,868)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">68)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">eturn false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">urn false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">ording to WHO classification, 2001

ding to WHO classification, 2001

ng to WHO classification, 2001

to WHO classification, 2001

o WHO classification, 2001

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O classification, 2001

classification, 2001

fication, 2001

cation, 2001

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Degree 0.The gland is not visible and not palpable.

Degree 0.The gland is not visible and not palpable.

pan class="">Degree 0.The gland is not visible and not palpable.

n class="">Degree 0.The gland is not visible and not palpable.

oid gland is well palpated

d gland is well palpated

gland is well palpated

and is well palpated

d is well palpated

is well palpated

well palpated

l palpated

palpated

span>

pan>

nlargement, are palpated.

argement, are palpated.

gement, are palpated.

ment, are palpated.

are palpated.

re palpated.

palpated.

ivssxtmus is visualized at swallowing

s is visualized at swallowing

is visualized at swallowing

isualized at swallowing

ualized at swallowing

lized at swallowing

/divv/tdlassssxthick neck" appearance

ck neck" appearance

neck" appearance

eck" appearance

uot; appearance

t; appearance

appearance

rowspanwspanpann"2>

he configuration of the neck

configuration of the neck

figuration of the neck

guration of the neck

ration of the neck

ivd><">

ed thyroid is visible in normal position of the neck.

thyroid is visible in normal position of the neck.

hyroid is visible in normal position of the neck.

d is visible in normal position of the neck.

is visible in normal position of the neck.

visible in normal position of the neck.

>

disfiguring goiter

isfiguring goiter

guring goiter

ring goiter

ng goiter

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3 3px;border:1px dotted #c0c0c0;cursor:hand;">urn false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">n false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">lse;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">e;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">cursor:hand;">rsor:hand;">hand;">nd;">;">

/p> > iv class="">Hormone level investigation of the hypophysis and the thyroid gland

lass="">Hormone level investigation of the hypophysis and the thyroid gland

ss="">Hormone level investigation of the hypophysis and the thyroid gland

="">Hormone level investigation of the hypophysis and the thyroid gland

Hormone level investigation of the hypophysis and the thyroid gland

rmone level investigation of the hypophysis and the thyroid gland

e level investigation of the hypophysis and the thyroid gland

level investigation of the hypophysis and the thyroid gland

vel investigation of the hypophysis and the thyroid gland

iv>

Detection of TSH and free fractions of T3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

Detection of TSH and free fractions of T3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

an class="">Detection of TSH and free fractions of T3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

class="">Detection of TSH and free fractions of T3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

lass="">Detection of TSH and free fractions of T3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

ns of T3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

of T3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

f T3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

T3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

sub>3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

b>3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

3 and T4 hormones with the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

the use of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

of modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

modern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

odern radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

n radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

radioimmunoenzymatic kits is the most exact method of research of the functional state of gland.

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

pan>

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

an>

Increase of TSH level is typical for the primary hypothyroidism of any etiology, decline - for the secondary hypothyroidism, hyperthyroidism.

Increase of free fraction of T4 (fraction of T4, which is not connected with blood proteins) is observed at hyperthyroidism, decline - at the decompensated hypothyroidism, deficit of iodine.

Increase of free fraction of T3 is observed at the decompensated hyperthyroidism and T3-toxicosis, decline - at the decompensated hypothyroidism.

Normal indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

al indices:

TSH 0.4-4.0 mIU/l

T4 total 65-146 nmol/l

T4 free 10-25 pmol/l

T3 total 1.2-2.8 nmol/l

T3 free 2.5-5.8 pmol/l

T3 free 2.5-5.8 pmol/l

sub>3 free 2.5-5.8 pmol/l

b>3 free 2.5-5.8 pmol/l

3 free 2.5-5.8 pmol/l

b> free 2.5-5.8 pmol/l

free 2.5-5.8 pmol/l

ree 2.5-5.8 pmol/l

r>

of the content of antibodies to thyroperoxidase, antibodies to thyroglobulin, to receptor ThTH (AB-rThTH)

the content of antibodies to thyroperoxidase, antibodies to thyroglobulin, to receptor ThTH (AB-rThTH)

he content of antibodies to thyroperoxidase, antibodies to thyroglobulin, to receptor ThTH (AB-rThTH)

content of antibodies to thyroperoxidase, antibodies to thyroglobulin, to receptor ThTH (AB-rThTH)

d>>These tests help to determine the autoimmune process activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

span class="">These tests help to determine the autoimmune process activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

an class="">These tests help to determine the autoimmune process activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

se tests help to determine the autoimmune process activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

tests help to determine the autoimmune process activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ests help to determine the autoimmune process activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

s help to determine the autoimmune process activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

help to determine the autoimmune process activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

lp to determine the autoimmune process activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

process activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

rocess activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

cess activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ss activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

activity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ctivity in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ty in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

in diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

n diffuse toxic goiter and autoimmune thyroiditis.

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

span class="">Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

an class="">Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

class="">Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

="">Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

">Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

Detection of autoantibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

antibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

tibodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

bodies to receptor TSH (TRAb) is executed for differential diagnostics of diffuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

fuse toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

se toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

toxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

oxic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ic goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

goiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

oiter, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

r, the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

the functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

he functional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

unctional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ctional autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

l autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

autonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

tonomy of the thyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

hyroid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

roid gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

id gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

gland.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

and.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

d.

Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

"">Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

>Increase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ncrease of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

rease of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ase of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

e of TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

TRAb level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

Ab level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

level at presence of clinical symptoms is the basic diagnostic criterion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

terion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

rion of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

on of diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

diffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ffuse toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

use toxic goitre, determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

determines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

etermines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ermines its severity and prognosis.

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

/p>

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

>

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

p>Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

pan class="">Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

n class="">Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ass="">Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

s="">Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

"">Normal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ormal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

mal indices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

dices:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ces:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

s:

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

>Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

span class="">Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

n class="">Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

class="">Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ass="">Antibodies to thyroperoxidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

xidase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

dase (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

se (AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

(AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

AB to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

to ThPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

hPO) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

O) 0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

0-35 IU/ml

Antibodies to thyroglobulin (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

in (AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

(AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

AB to ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

ThG) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

G) 0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

0-60 IU/ml

Antibodies to receptor TSH (TRAb) <2 IU/l

>

Antibodies to receptor TSH (TRAb) <2 IU/l

/p>

Antibodies to receptor TSH (TRAb) <2 IU/l

>

Antibodies to receptor TSH (TRAb) <2 IU/l

Detection of thyrocalcitonine content

p>Detection of thyrocalcitonine content

Detection of thyrocalcitonine content

pan class="">Detection of thyrocalcitonine content

n class="">Detection of thyrocalcitonine content

class="">Detection of thyrocalcitonine content

s="">Detection of thyrocalcitonine content

"">Detection of thyrocalcitonine content

>Detection of thyrocalcitonine content

ection of thyrocalcitonine content

tion of thyrocalcitonine content

f thyrocalcitonine content

thyrocalcitonine content

yrocalcitonine content

content

ntent

ent

span>

an>

d>

Normal indices:

Calcitonine 5.5-28 pmol/l

cancer of the thyroid gland

Normal indices:

Calcitonine 5.5-28 pmol/l

ncer of the thyroid gland

Normal indices:

Calcitonine 5.5-28 pmol/l

f the thyroid gland

Normal indices:

Calcitonine 5.5-28 pmol/l

the thyroid gland

Normal indices:

Calcitonine 5.5-28 pmol/l

e thyroid gland

Normal indices:

Calcitonine 5.5-28 pmol/l

span>

Normal indices:

Calcitonine 5.5-28 pmol/l

an>

Normal indices:

Calcitonine 5.5-28 pmol/l

>

Normal indices:

Calcitonine 5.5-28 pmol/l

p> iv>Detection of free cortisol content in daily urine

>Detection of free cortisol content in daily urine

etection of free cortisol content in daily urine

ection of free cortisol content in daily urine

tion of free cortisol content in daily urine

on of free cortisol content in daily urine

free cortisol content in daily urine

ree cortisol content in daily urine

e cortisol content in daily urine

d>v class

Its level goes down at primary and secondary suprarenal insufficiency, concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

p>Its level goes down at primary and secondary suprarenal insufficiency, concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

nal insufficiency, concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

l insufficiency, concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

insufficiency, concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

sufficiency, concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

fficiency, concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

iciency, concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

iency, concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

y, concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

concomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

oncomitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

mitant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

tant to some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

o some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

some diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

me diseases of the thyroid gland.

Normal indices:

60-413 nmol/day.

the thyroid gland.

Normal indices:

60-413 nmol/day.

e thyroid gland.

Normal indices:

60-413 nmol/day.

thyroid gland.

Normal indices:

60-413 nmol/day.

roid gland.

Normal indices:

60-413 nmol/day.

id gland.

Normal indices:

60-413 nmol/day.

gland.

Normal indices:

60-413 nmol/day.

lass="">Normal indices:

60-413 nmol/day.

ss="">Normal indices:

60-413 nmol/day.

="">Normal indices:

60-413 nmol/day.

">Normal indices:

60-413 nmol/day.

Normal indices:

60-413 nmol/day.

rmal indices:

60-413 nmol/day.

indices:

60-413 nmol/day.

dices:

60-413 nmol/day.

ces:

60-413 nmol/day.

/divv/td>

oid hormone (parathor-mone) content

d hormone (parathor-mone) content

hormone (parathor-mone) content

rmone (parathor-mone) content

one (parathor-mone) content

e (parathor-mone) content

arathor-mone) content

athor-mone) content

hor-mone) content

mone) content

ne) content

ntent

ent

t

It is executed at suspicion on the intraoperative trauma of parathyroid glands. Its level goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

span class="">It is executed at suspicion on the intraoperative trauma of parathyroid glands. Its level goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

an class="">It is executed at suspicion on the intraoperative trauma of parathyroid glands. Its level goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

a of parathyroid glands. Its level goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

of parathyroid glands. Its level goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

parathyroid glands. Its level goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

hyroid glands. Its level goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

roid glands. Its level goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

id glands. Its level goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

vel goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

l goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

goes down at the intraoperative parathyroid trauma.

Normal indices:

15-65 pg/ml.

pan class="">15-65 pg/ml.

n class="">15-65 pg/ml.

class="">15-65 pg/ml.

ass="">15-65 pg/ml.

s="">15-65 pg/ml.

"">15-65 pg/ml.

>15-65 pg/ml.

65 pg/ml.

pg/ml.

g/ml.

.

/span>

p> /tdb>>

f thyrotoxicosis (hyperthyroidism)

thyrotoxicosis (hyperthyroidism)

yrotoxicosis (hyperthyroidism)

otoxicosis (hyperthyroidism)

oxicosis (hyperthyroidism)

icosis (hyperthyroidism)

is (hyperthyroidism)

(hyperthyroidism)

hyperthyroidism)

rthyroidism)

hyroidism)

ism)

m)

divv>d>

conditioned by the pathological affecting organism of persistent surplus of thyroid hormones. This term is summarizing. It includes in itself the concept of the hyperthyroidism conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

onditioned by the pathological affecting organism of persistent surplus of thyroid hormones. This term is summarizing. It includes in itself the concept of the hyperthyroidism conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

oned by the pathological affecting organism of persistent surplus of thyroid hormones. This term is summarizing. It includes in itself the concept of the hyperthyroidism conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

ed by the pathological affecting organism of persistent surplus of thyroid hormones. This term is summarizing. It includes in itself the concept of the hyperthyroidism conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

by the pathological affecting organism of persistent surplus of thyroid hormones. This term is summarizing. It includes in itself the concept of the hyperthyroidism conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

cal affecting organism of persistent surplus of thyroid hormones. This term is summarizing. It includes in itself the concept of the hyperthyroidism conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

l affecting organism of persistent surplus of thyroid hormones. This term is summarizing. It includes in itself the concept of the hyperthyroidism conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

affecting organism of persistent surplus of thyroid hormones. This term is summarizing. It includes in itself the concept of the hyperthyroidism conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

dism conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

sm conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

conditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

onditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

ditioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

tioned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

oned by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

by hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

y hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

hyperproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

rproduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

roduction of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

ion of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

n of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

of hormones directly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

ectly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

tly in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

y in the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

n the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

the thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

e thyroid gland. In addition, thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

thyrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

yrotoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

otoxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

oxicosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

icosis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

osis can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

can be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

n be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

be conditioned by formation of hormones out of gland and special mechanisms of hormones' receipt in blood (drug, thyrolytic and other).

chanisms of hormones' receipt in blood (drug, thyrolytic and other).

anisms of hormones' receipt in blood (drug, thyrolytic and other).

isms of hormones' receipt in blood (drug, thyrolytic and other).

f hormones' receipt in blood (drug, thyrolytic and other).

hormones' receipt in blood (drug, thyrolytic and other).

rmones' receipt in blood (drug, thyrolytic and other).

n blood (drug, thyrolytic and other).

blood (drug, thyrolytic and other).

ood (drug, thyrolytic and other).

e>
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#c0c0c0;cursor:hand;">','rds|rds','popup_image(doc,ISBN9785970439272-0008,POPUP-Xz17-pic_0172.jpg,911,617)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">'rds|rds','popup_image(doc,ISBN9785970439272-0008,POPUP-Xz17-pic_0172.jpg,911,617)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">70439272-0008,POPUP-Xz17-pic_0172.jpg,911,617)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">439272-0008,POPUP-Xz17-pic_0172.jpg,911,617)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">9272-0008,POPUP-Xz17-pic_0172.jpg,911,617)');}return false;}" style="padding:3 3 3 3px;border:1px dotted #c0c0c0;cursor:hand;">divv classasss=div-tablev-tabletableble">Subclinical thyrotoxicosis (mild course)

span class="">Subclinical thyrotoxicosis (mild course)

dide (0.5-1.0 g every 12 hours). Beta-adrenoreceptors antagonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

a-adrenoreceptors antagonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

adrenoreceptors antagonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

noreceptors antagonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

receptors antagonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

eptors antagonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

tors antagonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

rs antagonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

tagonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

gonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

nists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

ropranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

pranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

f 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

very 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

urs (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

here is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

re is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

o cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

cular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

lar insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

r insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

fficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

iciency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

iency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

/span>

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

pan>

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

n>

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

>Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

n class="">Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

class="">Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

ass="">Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

ucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

ocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

icoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

oids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

ds: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

isone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

one intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

e intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

avenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

enously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

ously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

y at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

00 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

g every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

ours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

etoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

oxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

(infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

nfusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

usion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

erapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

apy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

pheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

eresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

esis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

is). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

edatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

atives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

s. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

he ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

the area of large vessels. In severe hypoxia - tracheostomy, ALV.

he area of large vessels. In severe hypoxia - tracheostomy, ALV.

ea of large vessels. In severe hypoxia - tracheostomy, ALV.

of large vessels. In severe hypoxia - tracheostomy, ALV.

f large vessels. In severe hypoxia - tracheostomy, ALV.

ls. In severe hypoxia - tracheostomy, ALV.

. In severe hypoxia - tracheostomy, ALV.

In severe hypoxia - tracheostomy, ALV.

ere hypoxia - tracheostomy, ALV.

e hypoxia - tracheostomy, ALV.

hypoxia - tracheostomy, ALV.

ypoxia - tracheostomy, ALV.

oxia - tracheostomy, ALV.

ia - tracheostomy, ALV.

- tracheostomy, ALV.

cheostomy, ALV.

eostomy, ALV.

my, ALV.

, ALV.

ALV.

pan>

n>

Lethality reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

p>Lethality reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

Lethality reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

an class="">Lethality reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

class="">Lethality reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

lass="">Lethality reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

ss="">Lethality reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

Lethality reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

thality reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

ty reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

eaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

0%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

he main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

ain cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

use of death is the multiple organ failure (cardiovascular, adrenal, liver).

e of death is the multiple organ failure (cardiovascular, adrenal, liver).

eath is the multiple organ failure (cardiovascular, adrenal, liver).

th is the multiple organ failure (cardiovascular, adrenal, liver).

is the multiple organ failure (cardiovascular, adrenal, liver).

the multiple organ failure (cardiovascular, adrenal, liver).

he multiple organ failure (cardiovascular, adrenal, liver).

multiple organ failure (cardiovascular, adrenal, liver).

ultiple organ failure (cardiovascular, adrenal, liver).

e organ failure (cardiovascular, adrenal, liver).

organ failure (cardiovascular, adrenal, liver).

failure (cardiovascular, adrenal, liver).

ailure (cardiovascular, adrenal, liver).

lure (cardiovascular, adrenal, liver).

ardiovascular, adrenal, liver).

diovascular, adrenal, liver).

ovascular, adrenal, liver).

ular, adrenal, liver).

ar, adrenal, liver).

, adrenal, liver).

renal, liver).

nal, liver).

l, liver).

er).

).

pan>

n>

p> >v classs="div-tablebleeableclassasssbl>p>Hypothyroidism

Hypothyroidism

pan class="">Hypothyroidism

ss="">Hypothyroidism

="">Hypothyroidism

">Hypothyroidism

Hypothyroidism

pothyroidism

thyroidism

/b>

>

/span>

p> Definition and statistical data

Definition and statistical data

>Definition and statistical data

class="">Definition and statistical data

ass="">Definition and statistical data

s="">Definition and statistical data

Definition and statistical data

finition and statistical data

nition and statistical data

tatistical data

tistical data

stical data

data

ata

a

pan>

n>

p> >p>Hypothyroidism is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

Hypothyroidism is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

pan class="">Hypothyroidism is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

ss="">Hypothyroidism is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

="">Hypothyroidism is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

">Hypothyroidism is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

othyroidism is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

hyroidism is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

roidism is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

sm is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

s a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

ndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

rome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

me caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

e caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

used by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

ed by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

eady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

yroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

oid gland hormones' insufficiency or their reduced biological effect at the tissue level.

nd hormones' insufficiency or their reduced biological effect at the tissue level.

hormones' insufficiency or their reduced biological effect at the tissue level.

ormones' insufficiency or their reduced biological effect at the tissue level.

es' insufficiency or their reduced biological effect at the tissue level.

' insufficiency or their reduced biological effect at the tissue level.

insufficiency or their reduced biological effect at the tissue level.

ficiency or their reduced biological effect at the tissue level.

ciency or their reduced biological effect at the tissue level.

ency or their reduced biological effect at the tissue level.

r their reduced biological effect at the tissue level.

their reduced biological effect at the tissue level.

eir reduced biological effect at the tissue level.

ir reduced biological effect at the tissue level.

reduced biological effect at the tissue level.

educed biological effect at the tissue level.

uced biological effect at the tissue level.

iological effect at the tissue level.

logical effect at the tissue level.

al effect at the tissue level.

effect at the tissue level.

ffect at the tissue level.

t the tissue level.

the tissue level.

e tissue level.

sue level.

e level.

level.

span>

an>

>
tdtd classassxt

Hypothyroidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

p>Hypothyroidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

n class="">Hypothyroidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

class="">Hypothyroidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

ass="">Hypothyroidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

s="">Hypothyroidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

"">Hypothyroidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

>Hypothyroidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

ypothyroidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

roidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

idism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

f various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

tiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

ology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

nd severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

rity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

ty degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

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Symptoms and treatment

Hyperthermia 39-40 °С., expressed perspiration.

Tachycardia to 200 in min, arrhythmia. Arterial hypertension to 200 mm Hg with high pulse pressure. Nausea, vomiting. Stomach-ache, hepatomegaly, jaundice.

Excitation, mental confusion. Then - sopor, coma.

Thiamazole (if unremoved thyroid gland) 20 mg every 4 hours via gastric probe. Preparations of iodine: i.v. a sodium iodide (0.5-1.0 g every 12 hours). Beta-adrenoreceptors antagonists: propranolol inside of 20-40 mg every 6 hours (if there is no cardiovascular insufficiency).

Glucocorticoids: hydrocortisone intravenously at a dose of 50-200 mg every 6 hours. Detoxification (infusion therapy 3-5 l / day, plasmapheresis). Sedatives. The ice on the area of large vessels. In severe hypoxia - tracheostomy, ALV.

Lethality reaches 50-60%. The main cause of death is the multiple organ failure (cardiovascular, adrenal, liver).

Hypothyroidism

Definition and statistical data

Hypothyroidism is a syndrome caused by steady thyroid gland hormones' insufficiency or their reduced biological effect at the tissue level.

Hypothyroidism of various etiology and severity degree in Russia occurs in about 19 out of 1000 women and in 1 out of 1000 men.

Classification

Types of hypothyroidism

Etiology

Primary hypothyroidism (thyrogenic)

Lack of functional activity of the thyroid gland:

- malformations (aplasia, hypoplasia);

- chronic autoimmune thyroiditis (the most common cause of hypothyroidism); other thyroiditis;

- after surgery on the gland, radioactive iodine therapy;

- excess thyreostatic therapy.

Violation of the thyroid hormones synthesis:

- congenital defects of thyroid hormone synthesis;

- iodine deficiency or an excess of iodine.

The toxic effects:

- some medicaments (drugs of lithium, interferons and others);

- other toxic agents.

Secondary hypothyroidism (hypophysial)

Organic and functional changes in the hypophysis, leading to reduced ThTH production (hypoplasia, tumorous, traumatic, radiation damages, cardiovascular and infectious lesions, toxic influences).

Tertiary hypothyroidism (hypothalamic)

Organic and functional changes in the hypothalamic centres, leading to reduced ThRH production (thyreoliberin).

The most commonly encountered in surgical practice is the primary hypothyroidism due to chronic autoimmune thyroiditis, surgery and treatment with radioactive 131I in various thyroid diseases.

Hypothyroid coma

Decompensation of protractedly existent hypothyroidism, manifested itself by disorders of respiratory and cardiovascular systems, by disorders of psyche.

Meets seldom, generally, at women of advanced age with primary hypothyroidism. Because of difficulties of diagnostics the lethality makes 40-70%.

Provoking and productive factors: overcooling, injuries, intoxications, and also inadequacy of a dose at the patients receiving treatment by thyroid hormones.

Symptomatology and diagnosis

Gradually within several weeks hypothyroidism symptoms accrue. Then join:

- hypothermia (body temperature <36 °С);

- bradycardia and hypotonia;

- polyserositis;

- acute urinary retention;

- sleepiness, violation of verbal contact, development actually of coma.

Diagnostics is difficult, especially in default of anamnestic data about the thyroid diseases and interventions on it.

All patients with coma in the presence of a hypothermia and hypoventilation are considered suspicious on a hypothyroidism. Free T3 and T4 are significant decreased. TSH, in most cases, are significantly increased (15-20 mkIE/ml).

Treatment

Treatment is in a reanimation separation. Correction of the main indicators of a homeostasis is necessary. Specific therapy consists in application of the thyroid hormones.

Syndrome of nodular goiter

Nodular (multinodular) goiter - a summarizing concept, including the great number of nosology units, the main feature of which are the focal masses determined visually, by palpation or by US. Each of these diseases is characterized by various mechanisms of an etiopatogenesis, morphological and clinical features, and also a different functional condition of the gland.

The clinical picture

At the small sizes of a nodal goiter the clinical picture is practically absent. At nodes of considerable size (more than 4-5 cm) and location of nodular goiter behind a breast there can be signs of compression of the trachea and esophagus: swallowing and breathing disorders, paresis of vocal cords. At the thyroid cancer the germination of surrounding fabrics is possible with a similar symptomatology. There are symptoms of hyperthyroidism at development of functional autonomy.

Displacement of trachea and esophagus is determined radiologically. Research of cervical lymph nodes (palpation, US) is obligatory.

Differential diagnostics and diagnosis

The diagnosis at nodular defeats of gland is defined, generally, by means of TNAB with the subsequent cytologic diagnostics. It allows to differentiate the diseases which are shown a nodular goiter. In some cases (at follicular neoplasia) histologic research is indicated. Thyroid scintigraphy, hormone profile allow to diagnose functional autonomy.

Variants of conclusions on results cytologic research of punctate obtained by means of thyroid TNAB

1. Nodular colloid goiter.

2. Follicular neoplasia: a) suspicion of malignancy; в) В-cellular; с) non-differentiated.

3. Thyroid gland cancer: a) papillary, follicular (including, from B-cells); в) medullary; с) anaplastic

4. Thyroiditis a) acute purulent; в) subacute (De Quervain); с) chronic autoimmune.

5. Cyst

6. Thyroid lymphoma.

7. Metastases of unthyroid tumors.

Characteristics of pathological processes in the thyroid

Pathological processes may occur on the background of iodine deficiency in the environment and its technogenic contamination. Some diseases are genetically determined. Another part is represented by tumor, autoimmune, inflammatory changes.

Morphological characteristics

Functional

Morphological changes of the gland may be of various character - diffuse, nodular, multinodular, mixed. These changes may be caused by colloid accumulation in the follicles, follicular epithelium hyperplasia, lymphoid infiltration, growth of connective or tumorous tissue. Up to 70% of diseases is a hyperplastic process (colloid proliferative goiter).

Diseases of the thyroid gland may develop on the background of normal functional activity (euthyrosis), increased functional activity (hyperthyrosis) and reduced functional activity (hypothyrosis).

The variety of etiopathogenic factors, morphological changes of the functional state and their combination leads to a lack of a single exhaustive classification of thyroid diseases.

THYROID DISEASES

Classification of the diseases of the thyroid gland on etiopathogenesis (one of variants)

Abnormalities of development

Abnormalities of sizes: aplasia and hypoplasia.

Abnormalities of localization:

- ectopic gland - the thyroid gland is in the usual place with additional sections of thyroid tissue in various organs and tissues (sublingual, retroesophageal localization);

- dystopia - the thyroid gland is not in its usual place, it can be located in the mediastinum, larynx, pharynx, paraesophageal.

Autoimmune diseases

Diffuse (mixed) toxic goiter - Graves's disease.

Chronic Hashimoto thyroiditis, painless ("silence"), postpartum, cytokine- induced thyroiditis

Endemic and sporadic goiter

Colloid proliferative goiter of different degrees:

1. diffuse euthyroid goiter

2. nodular and multinodular euthyroid goiter:

- without functional autonomy;

- with the formation of functional autonomy.

Tumors

Epithelial:

Benign:

- follicular adenoma

- from А-cells (more often),

- from oxyphil B-cells;

- cystic adenoma

Malignant: papillar cancer, follicular cancer, flat cell cancer, non-differentiated cancer, medullar cancer (from C-cells)

Non-epithelial:

Benign: fibroma, leiomyoma, hemangioma

Malignant: fibrosarcoma

Mixed tumors

Hemangio-endothelioma, teratoma, carcinosarcoma

Inflammatory

Acute thyroiditis, de Quervain's subacute thyroiditis

Specific lesions

Tuberculosis, syphilis, echinococcosis, actinomycosis, aspergillosis, candidiasis

Other

Fibrous Riedel's thyroiditis, amyloidosis, sarcoidosis

DIFFUSE TOXIC GOITER (DTG)

(SYNONYMS - BASEDOW'S DISEASE, GRAVES' DISEASE)

Definition and statistical data

DTG is an autoimmune disease characterized by thyroid hormones hyperproduction and steady increase of their content in the blood serum in combination with diffuse enlargement of the thyroid gland under the influence of specific autoantibodies with consequent impairment of various organs and systems condition. This disease is characterized by the most striking manifestations of the syndrome of thyrotoxicosis (hyperthyroidism).

The incidence of 5-6 cases per 100 thousand population. The disease occurs more frequently in women of 20-50 years old. The ratio between men and women being about 1:8-1:10. In the structure of all diseases of the thyroid gland it accounts for about 10%.

Sometimes it is necessary to carry out differential diagnostics with other diseases simulating signs of thyrotoxi-cosis - rheumatism (cardio-vascular syndrome), neurasthenia (syndrome of increased nervous excitement), tuberculosis (cachexia, subfebrility).

Ophthalmopathy may be conditioned not only by thyrotoxicosis, but also by other autoimmune processes, as well as by the impairment of the central nervous system.

Conservative treatment

Medicamentous

Radioiodotherapy

Means

Thyrostatics (drugs of tionamids, violates the synthesis of thyroid hormones) - thiamazole, carbimazole 30-40 mg / day, propylthiouracil 200-600 mg / day depending on severity of the toxicity. Sedative preparations (bromdihydrochlorphenylbenzodiazepine). β-adrenoreceptors antagonists (propranolol).

Hepatotropics (Silybi mariani fructuum extract, ademetionine, phospholipides)

Correction of electrolyte imbalance (polarizing mixture, magnesium as-partate and potassium aspartate). Prophylaxis and liquidation of adrenal insufficiency (prednisolone). To reduce the concentration of thyroid hormones, average mass molecules, antithyroid antibodies and underoxidized metabolic products can be used plasmapheresis. Cardiac glycosides (in blood circulation insufficiency), diuretics (in blood circulation insufficiency, ophthalmopathy), anabolic steroids (in pronounced catabolic syndrome) are used.

In order to improve oxygen balance hyper-barooxigenation (HBO) is used.

Peroral administration of radioactive iodine in gelatinous capsules, containing 10-15 mCu I131.

Benefits

Simplicity, non-invasiveness. Lack of severe complications.

Non-invasiveness. Minimal risk of recurrence

(up to 5%). Lack of severe complications.

Disadvantages

Duration of treatment (1.5-2 years). Limited application of thyrostatics in pregnant women.

High risk of recurrence (40-70%).

Development of hypothyrosis (up to 80%). Clinical effect is reached not earlier than 6 months following the dose of isotope. Limited application in young people. Possibility of planning preg-nancy not earlier than a year after treatment.

When failure of medical treatment of DTG (lack of stable remission), these same tools are used for preoperative preparation.

Surgery performed only when the medical euthyroidism is achieved.

Complications of surgical treatment of DTG

Complication

Clinical picture

Treatment

Bleeding

- of mild intensiveness

- Intensive

Abundant soaking of the dressing or accumulation in the vacuum - drainage container of not more than 50 ml of blood for an hour.

Cold load on the wound, hemostatic therapy.

Increasing hematoma and respiratory failure.

Surgical intervention - stopping of hemorrhage.

Paresis of the larynx

It is associated with uni- or bilateral

lesion of recurrent laryngeal nerves.

Aphonia without respiration disturbance.

Vitamins of the groups В, Е, prozerine, dibasole, voice gymnastics.

Aphonia with respiration disturbance, stridor.

Tracheostomy. Later on - operative correction of the vocal cords.

Hypoparathyrosis

It is associated with removal, trauma or ischemia of the parathyroid glands.

Hypocalciemia. Convulsions in the hands' fingers ("obstetrician hand"), trismus of masticatory musculature.

Calcium chloride intravenously. Peroral calcium preparations, dihydrotachysterol (AT-10).

Very rarely (if insufficient preoperative preparation) thyrotoxic crisis develops.

At reccurence of the disease after subtotal resection of the thyroid radioiodine therapy or thyroidectomy is indicated.

AUTOIMMUNE THYROIDITIS (АТ)

Definition and statistical data

Autoimmune thyroiditis is a chronic inflammatory disease of the thyroid gland of autoimmune genesis.

It makes about 20-30% of the diseases of the thyroid gland. More common in women (15-20 times more often than men) aged 40-50 years.

Diagnostics

Treatment

1.Examination, palpation - detection of various forms of the gland's transformation. At US - tissue hypoechogenity.

2. Increased TSH level at normal T4 level testifies subclinical hypothyrosis. Increased TSH level at reduced T4 concentration testifies clinical hypothyrosis.

3. Increased level of antithyroid antibodies in the blood (AB to ThPO, Th7).

4. At TNAB (it is performed in the presence of nodules to exclude cancer) - lymphocytes, fibroblasts.

At Hashitoxicosis - thyrostatics, β-adreno-blockators. During hypothyroid phase - substitutional hormonotherapy (L-thyroxin 50-100 mcg/day).

Indications to the operation: compression syndrome, cosmetic defect. Subtotal resection is usually performed, recently - thyroidectomy. At massive goiter in patients of poor condition with surrounding organs' compression - economic resection of the gland.

The main features of AT:

- primary hypothyrosis,

- hypoechogenity at US,

- antithyroid antibodies.

The diagnosis is confirmed by the presence of all three main characters.

Other types of thyroiditis (these occur rarely - up to 0.2% among the pathology of the thyroid gland)

Types

Definition

Etiology

Clinical picture

Treatment

Acute purulent thyroiditis

inflammation of the gland caused by purulent infec-tion penetrating through hematogenic and lymphogenic viae.

Endogenic infection (streptococcus, staphylococcus, etc.).

Tender swelling on the neck. Hyper-emia of the skin above the swelling. Hyperthermia of 38-40 °C.

Antimicrobial therapy. In abscess formation - opening and drainage of abscesses.

Acute non-purulent thyroiditis

Aseptic inflammation of the gland.

Traumas, radiation effect.

Diffuse enlargement of the gland, mild thyrotoxicosis.

Analgetics, β-adrenoblockators, NHAIP.

Subacute thyroiditis (De Quervain granulematous goiter)

Inflammatory disease of the thyroid gland caused by viral infection and secondary autoimmune process.

Viral infection. In destruction of thyrocytes antigen (thyroglobulin) is released which causes autoimmune inflammation.

Tender swelling on the neck. Hyperemia of the skin above the swelling. Mild thyrotoxicosis.

Glucocorticoids, NHAIP, β-adreno-blockators.

Fibrous Riedel's thyroiditis.

Impairment of the gland in visceral fibromatosis. It is combined with retroperitoneal, mediastinal fibroses, sclerosing cholangitis.

Growth of connective tissue substituting parenchyma in the thyroid gland.

Goiter of stone density, painless and almost immovable at palpation. With progressing of fibrosis hypothyrosis develops.

In large sizes of goiter with surrounding organs' compression - economic resection of the gland or thyroidectomy.

In diagnostics and differential diagnostics are helpful laboratory indices (detection of hormones' level), US, scintigraphy, TNAB (at nodulation), histologic research.

DIFFUSE EUTHYROID GOITER (DEG)

Definition and statistical data

DEG - diffuse enlargement of the thyroid gland without compromising its function, which is the main reason for the lack of iodine in the water of a certain region (endemic goiter). But it's possible DEG is outside areas of endemic goiter due to congenital or acquired defects in the biosynthesis of T3 and T4 (sporadic goiter).

More than 50% cases of the DEG develop before the age of 20.

The goiter is considered endemic in excess incidence of goiter in infants and school-age children more than 5%, and a median urinary iodine below 100 mg/l.

Etiopathogenesis

At DEG the increase in volume o the thyroid gland has compensatory character in response to a lack of iodine and is aimed at providing an organism with thyroid hormones.

In the pathogenesis of iodine deficiency goiter is set to increase production of TSH and increasing sensitivity to it of thyrocytes.

Along with this autocrine growth factors (ARF) - insulin-like growth factor type 1 (IGF-1), epidermal growth factor (EGF) and fibroblast growth factor (FGF) are important, which in the conditions of reduction of iodine in the thyroid have a stimulating effect on thyrocytes.

COLLOID NODULAR (MULTINODULAR) PROLIFERATIVE GOITER

Colloid nodular goiter - benign diseases of thyroid associated most often with a chronic deficiency of iodine in the environment. It does not exclude other mechanisms of its formation.

Among nodular thyroid is the most common (90%). The main contingent - women over 50 years.

Clinical picture and diagnosis

Complaints: usually absent. At a large goiter breathing problems, swallowing may be in the clinical picture. A node is detected visually, by palpation, US, TNAB - the predominance of a colloid, a different degree of proliferation of the follicular epithelium.

Cystic goiter is characterized by the presence of cavities filled with colloid.

Final diagnosis is possible on the basis of the TNAB data of nodules.

Colloid goiter is not susceptible to malignancy.

Treatment

At small sizws of colloid nodular goiter it is indicated the dynamic monitoring: determination of TSH (to except the functional autonomy), US (growth node control) 1 time per year.

Surgical treatment

It is indicated at large goiter size, the phenomenon of compression of the neck, gross cosmetic defects. Operation of selection - thyroidectomy, hemithyroidectomy available at the location node(s) in one lobe.

Radiation therapy with radioactive iodine

At the same indications, in the absence of contraindications.

Suppressive therapy with levothyroxine sodium is only possible for young people with a small node.

FUNCTIONAL AUTONOMY OF THE THYROID GLAND

Nodular toxic goiter (toxic adenoma - Plummer's disease) and multinodular toxic goiter

Definition and statistical data

It is an autonomously functioning adenoma (adenomas) of the thyroid gland which produces an excessive amount of thyroid hormones causing thyrotoxocosis.

In the structure of the thyroid gland diseases patients with toxic adenoma constitute about 9%. The disease occurs more frequently in women above 50 years living in goiter-endemic regions.

Classification of functional autonomy of the thyroid gland

By the number of autonomy formations

- unifocal,

- multifocal,

- disseminated (diffuse location in thyroid tissue autonomously functioning thyrocytes)

According to the severity of thyrotoxicosis

- compensated (in the absence of clinical symptoms of thyrotoxicosis),

- decompensated (if present)

Treatment

At the toxic nodular goiter thyrostatics have no lasting effect. After their withdrawal symptoms reappear thyrotoxicosis.

At the compensated functional autonomy an annual survey of the patient is indicated.

Methods of treatment of decompensated functional thyroid autonomy

Surgical (main).

Hemithyroidectomy with isthmusectomy is at unifocal autonomy, thyroidectomy - at multifocal and disseminated forms.

Radioiodotherapy (it is often accompanied by the development of hypothyrosis).

Transcutaneous sclerosing therapy with ethanol, radiofrequency thermodestruction (rarely used).

Preoperative therapy involves thyrostatics to achieve euthyroidism, as well as symptomatic cardiotropic and sedative therapy.

Application of the methods of destruction of local nodes (ethanol ablation, radiation ablation) has not statistically proven benefits.

FOLLICULAR ADENOMAS

Clinical picture

It is absent or at large sizes by causing compression of the neck (trachea, esophagus).

On examination, tumor formation can be determined with the intact skin. Palpation painless. The contours of the node are distinct, the surface is smooth, elastic consistency. Regional lymph nodes are not enlarged.

US

Rounded formations with clear contours, manifest capsule.

Scintigraphy

"Cold" node

TNAB

The differentiation of follicular adenoma and follicular cancer according to TNAB is impossible.

Variants of cytological results at the follicular tumor:

- follicular neoplasia;

- neoplasia from Askanazy-Huerthle cells.

Treatment

In most cases, either in clinical or in laboratory tests, including TNAB, it is impossible to distinguish between follicular adenoma and follicular cancer. Therefore, surgery is indicated with an urgent histological examination. However, it does not always provide an unambiguous result. Because of this, a hemithyroidectomy with isthmusectomy is made.

THE THYROID GLAND CANCER

The thyroid gland cancer - a malignant nodular formation that develops from follicular (A and B - cells) or epithelial parafollicular (C-cells) of the thyroid gland.

The frequency of the prevalence of thyroid cancer is about 1.5% of all malignant tumors of other localizations. It is diagnosed in 5-6% of patients with thyroid nodules. More common in women after 40-60 years

(3.5 times more likely than men).

Risk factors

General or local X-ray or ionizing radiation (especially during childhood and adolescence). Some hereditary genetic diseases (familial polyposis, Gardner's syndrome, familial forms of medullary thyroid carcinoma and others).

According to origin and histological structure

According to origin and histological structure

From A-cells, B-cells

From C-cells

Papillar cancer (60-70%)

Follicular cancer (20-30%)

Aplastic (non-differentiated) cancer (5-10%)

Medullar cancer (4-6%)

Classification according to system TNM (UICC, 2009)

ТХ

The primary tumor can not be assessed

T0

The primary tumor is not detected

T1

The tumor is 2 cm or less, limited by thyroid tissue

Т1а

The tumor is not more than 1 cm, limited by thyroid tissue

T1b

The tumor is 1-2 cm, limited by thyroid tissue

T2

The tumor is 2-4 cm, limited by thyroid tissue

T3

The tumor is more than 4 cm, limited by thyroid tissue or tumor of any size with a minimum spread beyond the thyroid capsule

T4a

The tumor spread beyond the thyroid capsule and enters the subcutaneous soft tissues, larynx, pharynx, trachea, esophagus, recurrent laryngeal nerve

T4b

The tumor penetrates prespinal neck fascia, mediastinal vessels or the common carotid artery

All anaplastic thyroid carcinomas are always classified as stage T4.

T4a - non-differentiated carcinoma localized within the thyroid gland - surgically resectable;

T4b - non-differentiated carcinoma spreading outside the limits of the thyroid gland - surgically non-

resectable.

Multiple tumors (multifocal) are further indicated by the letter m, thus crucial has the largest tumor size, e.g., T2 (m)

NX

there are no sufficient data for evaluation of regional lymph nodes

N0

there is no metastatic lesion of regional lymph nodes;

N1

There are metastases into regional lymph nodes

N1a

Level VI metastases (pre- and paratracheal, prelaryngeal)

N1b

Metastases are in lateral cervical lymph nodes (I-V) on the side of thyroid lesions and / or on the opposite or upper mediastinal lymph nodes

M0

there are no signs of distant metastases

M1

there are distant metastases

Classification of the thyroid cancer according to stages (UICC, 2009)

Papillary and follicular cancer in patients younger than 45 years old

Stage I

Any Т

Any N

M0

Stage II

Any Т

Any N

М1

Papillary and follicular cancer in patients 45 years and older, and medullary cancer

Stage I

Т1

N0

M0

Stage II

Т2

N0

Stage III

Т1, Т2, Т3

N0, N1a

Stage IVa

Т1, Т2, Т3, Т4а

N0, N1, N1b

Stage IVb

Т4Ь

Any N

Stage IVc

Any Т

M1

Non-differentiated (aplastic) cancer

Stage IVa

Т4а

Any N

M0

Stage IVb

Т4Ь

Stage IVc

Any Т

M1

Treatment

At follicular and papillary carcinoma, manifested by solitary microcarcinoma (T1 N0 M0), it is allowed the hemithyroidectomy with isthmusectomy. In other cases, it is performed extrafascial thyroidectomy, bilateral cervical lymphodissection.

At presence of regional metastases fascial-case neck dissection is produced with moving away of pretracheal, paratracheal, prelaryngeal, supraclavicular lymphatic nodes.

At the germination of thyroid cancer in the internal jugular vein it is performed Kreil's operation (thyroidectomy, fascial-case lymphodissection, resection of the vein).

At the equivocal TNAB (follicular neoplasia) the final volume of the operation is determined after histological conclusion. Urgent intraoperative research is not always informative, so in some cases repeated interventions are carried out after planned histological examination.

Postoperative treatment of patients

Operation at papillary and follicular cancer is added by radioiodotherapy.

Distant radiation therapy is carried out in cases of aggressive tumors, at impossibility of radical operation. Suppressive therapy with thyroxine (STT) - used after thyroidectomy to suppress the stimulating effect of TSH.

Identification of thyroglobulin in the blood after removal of the thyroid gland is considered to be the most informative tests to detect recurrence of papillary and follicular cancer (cells capture 131I). The cells of medullary carcinoma preserve the capacity to produce calcitonine, that is why the detection of calcitonine concentration in the blood is used to identify recurrence and metastasis.

Prognosis of the results of ThGC treatment

Form

Differentiation

Survival rate

Papillar and follicular

Highly differentiated

10 years - 91-93%

Medullar

Moderately differentiated

10 years -55-6O%

Anaplastic

Poorly differentiated

5years - 5-6%

PATHOLOGY OF THE ABNORMALLY LOCATED THYROID GLAND

Among the anomalies location there are distinguished ectopic thyroid and dystopia.

Ectopia - a defect of embryonic thyroid bookmark. In addition to the normally located ThG there are additional sections of thyroid tissue from the root of language to the level of the aortic arch (aberrant thyroid gland).

Dystopia - a vicious bookmark of ThG as a result of a disembryogenesis, in this connection its basic location changes.

Aberrant gland are located in the tongue basis, between the jugular incisure and the isthmus of the gland, in the mediastinum, in the larynx or pharynx, in the heart bag.

Dystopic thyroid is located in the mediastinum, larynx, pharynx, esophagus area. It is extremely rare (up to 0.3% of cases) In sublingual localization the thyroid gland in the typical place is lacking in 70% of patients. Sometimes thyroid tissue is composed of ovaries - struma ovary. It refers to the teratoma, not to anomalies of embryogenesis.

Clinical picture, diagnostics and treatment

Retrosternal goiter

The source of retrosternal goiter is the low located thyroid gland. It often develops at the normally located gland. Emerging nodes in the lower pole is gradually lowered behind the sternum. The negative intrathoracic pressure helps goiter lowering. At coughing the goiter moves up and out of the jugular incisure of the sternum (diving, wandering goiter). Expansion of veins of neck is possible because of compression by the superior vena cava. At lifting the arms above the head there are hyperemia of face, dizziness or fainting (Pemberton's symptom).

Intrathoracic goiter

It develops in the anterior mediastinum out of ectopic tissue of the thyroid gland. From 5 to 40% of patients have no complaints. Clinical manifestations are conditioned by constriction or dislocation of the surrounding organs: breathlessness, dry cough, dysphagia, change of voice, syndrome of superior vena cava (Pemberton's symptom).

Sublingual goiter

There are symptoms of thyroid dysfunction and symptoms of local compression of the pharynx, the epiglottis.

Retroesophageal goiter

Difficulty in swallowing due to the esophagus dislocation is possible.

Struma ovary

Consists of thyroid tissue and, in most cases, it proceeds with symptoms of hyperthyroidism. It may also be the source of malignant transformation of cells.

Diagnostics is based on the clinical picture and it is verified with the help of scintigraphy, CT, NMRI.

In case the clinical manifestations are present surgical treatment is used - thyroidectomy by the access through the neck, sometimes by sternotomy or the combined access.