www.endotext.org/chapter/multinodular-goiter/
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nherited Defects In Thyroid Hormone Synthesis And Resistance To Thyroid Hormone Action
TSH released from the thyrotrophs will continuously stimulate the thyroid gland growth
most cases of familial goiter present an autosomal dominant pattern of inheritance
It was also found that, while being still within the normal range, the mean serum T3 concentration of the group with impaired TSH secretion was significantly higher than the normal mean, whereas the mean value of serum T4 levels was not elevated
Nodular goiter may be the result of any chronic low-grade, intermittent stimulus to thyroid hyperplasia
thyroid first goes through a period of hyperplasia as a consequence of the resulting TSH stimulation, but eventually, possibly because of iodide repletion or a decreased requirement for thyroid hormone, enters a resting phase characterized by colloid storage and the histologic picture of a colloid goiter
By the time the goiter is well developed, serum TSH levels and TSH production rates are usually normal or even suppressed
Gender (women) is an important factor
Subsequent functional and structural abnormalities in growing goiters
Elevated TSH
Smoking, stress, certain drugs
Other thyroid-stimulating factors
Stimulation of new follicle generation seems to be necessary in the formation of simple goiter
Evidence accumulated from many studies indicates that iodine deficiency or impairment of iodine metabolism by the thyroid gland
important mechanism leading to increases in TSH secretion
Since in experimental animals the level of iodine per se may modulate the response of thyroid cells to TSH
this
additional mechanism by which relatively small increases in serum TSH level may cause substantial effects on thyroid growth in iodine-deficient areas
found that the thyroidal iodine clearance of patients with nontoxic nodular goiter was, on overage, higher than that in normal persons
finding
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