87. Thyroid hypofunction.

Aethiology:

1) central disorders: thyreoliberine and TTH synthesis and secretion decreasing due to hypothalamus and adenohypophysis (secondary hypothyreosis) disorders;

2) glandular disorders leadin to primary hypothyreosis development:

a) thyroid tissue decomposition for instance with radioactive iodum;

b) iodum deficiency in drinking water and food – endemic goiter;

c) thyroid autoimmune injury – autoimmune thyreoiditis of Hashimoto;

d) congenital disorders – thyroid hypo- and aplasy, enzymopathies;

3) peripheral disorders:

a) peripheral cells non-sensitivity to thyreoid hormones action;

b) thyreoid hormones enforced binding with blood plasma proteins;

c) their enforced metabolism in liver.

Pathogenetic mechanisms:

1) Tissues growth and differentiation disorders:

a) lack of anabolic effects and STH secretion decrasing;

b) bones growth in length is disordered because thyroid hormones are essential for enchondral ossification on boarder between dyapphisis and epiphysis; periostal growth remains non-changed and bones are thick;

c) hypothyreoid dwarfness is developed;

d) mental development is retarded – cretinism is developed (in children).

2) Thyreoid hormones heat-producing action reducing:

a) basal exchange is decreased on 20-40% because of biological oxidation weakening in mitochondria and excitive tissues functional activity;

b) heat-production decreasing which leads to temperature falling down;

c) bad adaptation to coldness while good adaptation to high temperature;

d) hypophagy – little energy consumption.

3) Excitive tissues functional activity reducingis connected with Na-K-ATPases activity decreasing and ions active transport changing. On other hand, tissues sensitivity to catecholamines is reduced because beta-adrenoreceptors quantity is decreased on cells. Functional changings of excitive organs and tissues are in following:

a) CNS activity disorders – mntal activity retardation, weakness, inhibiting, sleepness;

b) skeletal muscles functional activity reducing – weakness, hypotony, rapid fatigueability;

c) cardiac-vascular system activity changings – bradycardy, heart minute volume diminishing, arterial hypotony;

d) intestines smooth muscles contractive function decreasing – constipations;

e) absorbtion and excretion processes disorders; glucose hypoabsorbtion in intestines leads to hypoglycaemia; cholesterol excretion disorders in bile content leads to hypercholesterolemia and further to atherosclerosis.

4) Disorders with unknown developmental mechanism. Mucous oedema or mixedema beongs to them. It is characterized by increasing in glycosaminoglycans binding water, skin thickness, oedematic face. There is a hypothesis according to which myxedema is a result of TTH action to connective tissue (TTH level is strongly increased at glandular and peripheral hypothyreosis forms).

Goiter is thyroid visible increasing. There can be hyperthyreoid, euthyreoid (sporadic and hypothyreoid at which thyroid function is increased, non-changed and decreased correspondingly.

Hypothyreoid goiter is endemic one. It is expressed in clinics of thyroid hypofunction. Its reason is iodum insufficient level in drinking water and goods which is connected with soil and subground water peculiarities in definite regions of Earth. Iodum deficiency lead to thyreoid hormones synthesis disorder the level of which is decreased in blood. It causes thyreoliberine and TTH production enforcement. TTH while its action to thyroid tissue simulates processes of hypertrophy and hyperplasy – goiter is developed. Since gland increasing doesn’t liquidate thyreoid hormones deficiency (the reason – iodum deficiency – is still present) than increased TTH production is remained and its action is keeping on to gland tissue – goiter is in progress.

Hashimoto’s autoimmune thyreoiditis – (he is discovered and described by Japanian surgeon in 1912) is the mostly widely spread among thyreoidites. Women of young and adult age are 95% of patients. 10% of female population suffers from it. Often – in adolescents on then background of juvenile hyperplasia because thyreocytes proliferation triggeres growth-stimulating autoantibodies against proteinic epitopes of thyreoid hormone receptor. There can also be family hereditary form of goiter. Thyreocytes express under goiter conditions aberrant antigens MHC II class absent in norm. Against them – autoantibodies. Cytokines increase expression of these antigens. Hypofunction of thyroid.

Radiation injury – radioactive I¹³¹ or Sr will be involved in hormones structure. Synthesis and function of them will be suffered.