Tyrosine is the amino acid upon which the thyroid hormones are based.
TSH is not really very species specific. (Good thing for all the TSH stimming that goes on.) TSH is made of 2 subunits TSH alpha & TSH beta. TSH alpha is common to LH & HCG. The second subunit is responsible for function.
TSH is secreted by the basophil cells of the adenohypophysis.
The real name of T3 is triiodothyronine.
Thyroglobulin is a large glycoprotein that stores T4 & T3 inside the thyroid gland. It is synthesized by thyroid cells & secreted in the colloid (protein rich fluid inside the thyroid follicles) T4 & some T3 are synthesized in the colloid & bound to thyroglobulin. When it is time for secretion, the thyroidcells ingest the colloid breaking the T3 & T4 off of the thyroglobins.
TSH stimulates both thyroid hormone production AND secretion. It also makes thyroid cells under go both hypertrophy & hyperplasia.
You get a goiter by having too much TSH. You could do this by having an iodine deficient diet (TSH is desparately trying to stimulate the thyroid but there's no substrate for hormone production), or if you have hypothyroidism (TSH is trying to stimulate a wimped out gland). I suppose if you had the right kind of pituitary tumor you could over produce TSH.
*Note: the large thyroid of a hyperthyroid cat is not a goiter. It is an adenoma which is different.
The three proteins which transport thyroid hormone are:
1) Thyroxine binding globulin (this is the only one T3 binds to ) 2) Thyroxine binding prealbumin 3) albumin
No, T3 doesn't do the receptor dance that way. It's more like a steroid hormone. T4 gets to actually enter the cell where it is converted to T3 by a deiodinase.
Myxedema is an acculmulation of mucin in the dermis & subcutis. The mucin binds water & the skin thickens markedly. This is most obvious on the face (tragic expression) Myxedema does not pit, unlike other edemas.
There are 4 parathyroids.
The two types of parathyroid epithelial cells are:
Chief cells (which secrete PTH) Oxyphil cells (no one knows what they do)
Calcitonin comes from the "C" cells (also called "parafollicular cells") of the thyroid.
FIRST MECHANISM: there is decreased renal phosphate excretion & phosphate is building up. According to mass action law Ca x PO4 = K. If PO4 goes up then Ca must go down. If Ca goes down, PTH is stimulated.
SECOND MECHANISM: In renal disease, activation of vitamin D is impaired (this process takes place in the kidney). A functional vitamin D deficiency leads to reduced Ca & PTH again gets stimulated.
THIRD MECHANISM: Like we said, phosphate levels are rising due to decreased renal excretion. Excess PO4 is getting excreted into the GI tract. In the GI tract PO4 is binding to calcium & precipitating out. This Ca doesn't get absorbed. Less Ca absorption from the intestine drops blood Ca & PTH is stimulated yet again.
One way (the classical way, I guess) is to eat an all-meat diet. (A Ca deficient diet).
Another way would be to eat a PO4 rich diet (though I don't know what that might be).
And the last way would be to get a Vitamin D deficiency.
In pseudohyperparathyroidism a tumor produces a PTH-like substance. Anal sac adenocarcinomas do the same thing.
