The most common cause of simple goiter is the absence of sufficient amounts of iodine in the diet.
As a consequence of lack of iodine in the diet, there is insufficient production of throid hormones.
This results in a feed-back increase in the synthesis and release of TSH (thyroid stimulating hormone), resulting in enlargement of the thyroid.
In the early stages of the disease, the thyroid is grossly symmetrically enlarged and appears uniform.
Due to processes that are incompletely understood, this stage of uniform enlargement of the thyroid is soon replaced by differential growth and involution of areas of the thyroid giving rise to the typical multinodular appearance.,
In areas of the world, primarily hilly regions where salt is obtained from the soil rather than from the sea, evidence of hypothyroidism is endemic.
|General Gross Description|
A multinodular thyroid is significantly larger than normal.
The normal thyroid weighs approximately 30 grams; a multinodular goiter can weigh several hundred grams.
On cut surface, the multinodular appearance is obvious, with numerous nodules of differing consistencies separated by fibrous septa.
Glassy appearing colloid is obvious in many of these nodules.
|General Microscopic Description|
Microscopically, the lesion is typified by follicles of varying sizes that appear quiescent.
Abundant colloid is seen in many of these hugely distended follicles.
Areas of hemorrhage and irregular calcification may also be seen.
The lining epithelium is slow cuboidal.
Multinodular goiter is the end stage in the evolution of simple goiter.
The most obvious feature of a goiter is the enlargement of the thyroid, that can often be seen an palpated.
Extreme enlargement of the thyroid can give rise to pressure symptoms on both the trachea and the esophagus.
Most patients with multinodular goiter are euthyroid; however, in endemic areas, where the disease is a result of insufficient iodine in the salt, many children are hypothyroid.
The tragic (and completely avoidable) consequence of neo-natal thyroid insufficiency is cretinism.
Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 1132
Harrison's Principles of Internal Medicine, 13th Ed: Isselbach et. al. (eds). New York, McGraw-Hill, 1994, pp.1940
|Synopsis by: T.V.Rajan, M.D., Ph.D. (T96000M71620)|
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