88. Hypothyroidism.

Reasons:

1) Central disorders – thyreolyberine and TTH secretion increasing at hypothalamus and adenohypophysis hyperfunction (secondary hyperthyreosis);

2) Glandular disorders (primary hyperthyreosis):

a) diffuse toxic goiter (Grevs’ disease, disease fon Bazed);

b) thyroid adenomas.

Diffuse toxic goiter is considered to be autoimmune disorder in the origin of which TTH-mimetic antibodies (with TTH action while interaction with thyrocytes superficial antigens – it is Vth type of allergy reactions by Kums and Jell). Such antibodies are known as LATS (long acting thyroid stimulators) and TSI (thyroid stimulating immunoglobuline) which possess the ability to interact with TTH-receptors. As these antibodies have no complement-binding locuses, than thyrocytes are not injured but function actively.

3) Perypheral disorders:

a) cells sensitivity increasing to T3 and T₄;

b) thyreoid hormones binding decreasing with transport proteins;

c) thyreoid hormones metabolism retardation in liver at its failure.

Pathogenetical mechanisms:

1) Antianabolic effects (highly-dosed):

a) growth retardation;

b) muscular atrophy and weakness;

c) body weight loosing;

d) negative nitrogen balance.

2) Heat-producing activity increasing:

a) basal exchange activation;

b) heat-production activating and body temperature rising up;

c)good adaptation to coldness and bad – to warmth;

d) hyperphagy.

3) Excitive tissues functional activity increasing due to Na-K pumps of cellular membranes hyperactivity and cells sensitivity increasing to catecholamines:

a) CNS hyperexcitability, insomnia;

b) constant spontaneous activity of muscular fibers – thremor; fatigueability and weakness are delt with it;

c) sympathetic effects to cardiac-vascular system;

d) intestinal smooth muscles hyperactivity – diarrhea;

e) hyperglycaemia and hypocholesterolemia due to absorbtion and exretion activation.

4) Catecholaminic effets because of cells sensitivity increasing to catecholamines due to beta-adrenoreceptors quantity increasing on their surface:

a) glycogenolysis activation in liver→hyperglycaemia→thyroid diabetes mellitus;

b) lipolysis activation in fatty tissue→hyperlipacydemia→ketogenesis activation in liver→metabolic acidosis;

c) non-phosphorylating oxidation activating in brown fatty tissue→heat production activation→temperature and basal exchange rising up.

5. Disorders with unknown reason:

1. orbitopathy (eye symptoms);

2. exophthalm.

Basement – eyeball muscles and retrobulbar tissue edema and lymphoid infiltration. These changings do not depend on thyroid hormones level in blood and on TTH_mimetic antibodies (LATS, TSI) concentration. It was thought about special excophthalmic factor but it is not still discovered.

Calcitonine is proteinic hormone of thyroid. Its production can be injured at thyreoidctomy, thyrostatics action and hyperthyreosis (endogenic and exogenic). Some cases of calcitonin excessive secretion are connected with tumors origined from interfollicular C-cells of thyroid, locus of its production. Non-real hypoparathyreosis is delt with calcitonin hypoproduction. Parathyroid glands functioning is normal but hypocalcaemia and phosphoric-potassium exchange disorders take place.

Calcitonin contains 32 aminoacids. M=36000 D. Main organ-target is osseal tissue. It inhibits Ca resorbtion (it is accompanied by hypocalcaemia) and P (hypophosphatemia) from osseal tissue. This peculiarity is actual during periods with increased needs in Ca (bones growth in children and adolescents, pregnancy, lactation). Hormonal secretion depends on Ca level in blood: hypercalcimia increases calcitonin synthesis, hypocalcaemia –inhbits. N level of calcitoninc in plasma in 0,002-0,4 ng/ml. It is parathyrin antagonist.