Goiter colloid

An increase in thyroid weight and incidence of colloid goiter are useful in the diagnosis of iodine excess. The finding of goitrous foals from mares consuming a highly iodized feed (Baker and Lindsey, 1968) is justifiably a frequently cited example of iodine excess in domestic animals. 

Birds and mammals exposed to PCB mixtures frequently react differently. PCBs generally elicit large-colloid goiters in birds these goiters are inherently different from hyperplastic goiters produced in mammals exposed to PCBs. Fish-eating seabirds, such as the razorbill (Alca torda), can rapidly metabolize PCB congeners that have at least one pair of adjacent unsubstituted metapara combinations in the biphenyl moiety. Razorbills metabolized 4-chlorobiphenyl to 4-chloro-4 hydroxybiphenyl however. 

The thyroid gland possesses a proteolytic enzyme this was first demonstrated by De Robertis (1941) in follicular colloid extracted from single follicles of rats thyroids the proteolytic activity of the enzyme was increased after the administration of thyrotropin and was decreased after administration of iodide. The activity of the enzyme was shown (De Robertis and Nowinski, 1946) to vary in different pathological conditions in human beings in cases of severe toxic goiter it was increased to twice the normal activity in simple colloid goiter it was appreciably lowered. 

Human fetuses in regions of severe endemic goiter have hyperplastic colloid goiters with no evidence of thyroid atrophy or destruction (22). 

Relative Puberty, adolescence, pregnancy, lactation it usually leads to colloid goiter, sometimes to nodular goiter... 

Figure 42-11. Model of iodide metabolism in the thyroid follicle. A follicular cell is shown facing the follicular lumen (top) and the extracellular space (at bottom). Iodide enters the thyroid primarily through a transporter (bottom left). Thyroid hormone synthesis occurs in the follicular space through a series of reactions, many of which are peroxidase-mediated. Thyroid hormones, stored in the colloid in the follicular space, are released from thyroglobulin by hydrolysis inside the thyroid cell. (Tgb, thyroglobulin MIT, monoiodotyrosine DIT, diiodotyro-sine Tj, triiodothyronine T4, tetraiodothyronine.) Asterisks indicate steps or processes that are inherited enzyme deficiencies which cause congenital goiter and often result in hypothyroidism.

Each step in the synthesis of thyroid hormones is regulated by pituitary TSH. TSH stimulates the iodide pump, Tg synthesis, and colloidal uptalce by foUicular cells. TSH also regulates the rate of proteolysis of Tg for the fib-eration of T4 and T3 is also regulated by TSH. In addition, TSH induces an increase in the size and number of the thyroid foUicular ceUs. Prolonged TSH stimulation leads to increased vascularity and eventual hypertrophic enlargement of the thyroid gland (goiter). 

At histology, goiters harbor microfollicular patterns, scant colloid and sometimes aberrant nuclei. The degree of hyperplasia in many areas is high and sometimes suggestive of malignant neoplasia. The association of thyroid cancer has... 

Chronic excessive iodine supplementation could cause goiter or retention of colloid in the thyroid. 

Swiss authors (2, 17) reported that neurological cretins have hyperplastic, colloid, multinodular goiters similar to those seen in non cretin individuals in the same area. They showed that myxedematous endemic cretins have thyroid atrophy and sclerosis. As a consequence of their thyroid failure, myxedematous cretins also have hyperplastic pituitary glands. 

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