Diffuse and Multinodular Goiters
Diffuse and multinodular goiters reflect impaired synthesis of thyroid hormone, most often caused by dietary iodine deficiency
Impairment of thyroid hormone synthesis leads to a compensatory rise in the serum TSH level, which, in turn, causes hypertrophy and hyperplasia of thyroid follicular cells and, ultimately, gross enlargement of the thyroid gland.
? The compensatory increase in functional mass of the gland is able to overcome the hormone deficiency, ensuring an euthyroid metabolic state in the vast majority of individuals. The degree of thyroid
? enlargement is proportional to the level and duration of thyroid hormone deficiency
DIFFUSE NONTOXIC (SIMPLE) GOITER
diffusely involves the entire gland without producing nodularity.
the term colloid goiter has been applied to this condition
Endemic goiter occurs in geographic areas where the soil, water, and food supply contain only low levels of iodine.
The lack of iodine leads to decreased synthesis of thyroid hormone and a compensatory increase in TSH, leading to follicular cell hypertrophy and hyperplasia and goitrous enlargement.
Sporadic goiter occurs less frequently than does endemic goiter. There is a striking female preponderance and a peak incidence at puberty or in young adult life. Sporadic goiter can be caused by a number of conditions,
Morphology.
Two phases can be identified the hyperplastic phase and the phase of colloid involution the hyperplastic phase, the thyroid gland is diffusely and symmetrically enlarged, although the increase is usually modest, The follicles are lined by crowded columnar cells, which may pile up and form projections similar to those seen in Graves disease.
The accumulation is not uniform throughout the gland, and some follicles are hugely distended, whereas others remain small. If dietary iodine subsequently increases or if the demand for thyroid hormone decreases, the stimulated follicular epithelium involutes to form an enlarged, colloid-rich gland (colloid goiter). the cut surface of the thyroid is usually brown, somewhat glassy, and translucent.
MULTINODULAR GOITER
recurrent episodes of hyperplasia and involution combine to produce a more irregular enlargement of the thyroid, termed multinodular goiter
They may be nontoxic or may induce thyrotoxicosis (toxic multinodular goiter). Multinodular goiters produce the most extreme thyroid enlargements and are more frequently mistaken for neoplastic involvement than any other form of thyroid disease
It is believed that multinodal goiters may arise because of variations among follicular cells in responses to external stimuli With uneven follicular hyperplasia, generation of new follicles, and uneven accumulation of colloid, tensions and stresses are produced that lead to rupture of follicles and vessels followed by hemorrhages, scarring, and sometimesThe scarring adds to the tensions, and in this cyclical manner, nodularity appears.
cut section, irregular nodules containing variable amounts of brown, gelatinous colloid are present
The microscopic appearance includes colloid-rich follicles lined by flattened, inactive epithelium and areas of follicular epithelial hypertrophy and hyperplasia, accompanied by the degenerativeThe dominant clinical features of goiter are those caused by the mass effects of the enlarged gland. In addition to the obvious cosmetic effects of a large neck mass, goiters may cause airway obstruction, dysphagia, and compression of large vessels in the neck and upper thorax. Most patients are euthyroid,
Neoplasm s of the Thyroid
? Several clinical criteria might provide a clue to the nature of a given thyroid nodule:
? • Solitary nodules, in general, are more likely to be neoplastic than are multiple nodules.
? • Nodules in younger patients are more likely to be neoplastic than are those in older patients
Nodules in males are more likely to be neoplastic than are those in females
A history of radiation treatment to the head and neck region is associated with an increased incidence of thyroid malignancy
Nodules that take up radioactive iodine in imaging studies (hot nodules) are more likely to be benign than malignant
ADENOMAS
are typically discrete, solitary masses
called follicular adenomas, the vast majority of adenomas are nonfunctional, toxic adenoma
Pathogenesis:The TSH receptor signaling pathway plays an important role in the pathogenesis of toxic adenomas. clonal expansion of follicular epithelial cells that can autonomously produce thyroid hormone and cause symptoms of thyroid excess
The typical thyroid adenoma is a solitary, spherical, encapsulated lesion that is well demarcated from the surrounding thyroid parenchyma. Follicular adenomas average about 3 cm in diameter, but some are smaller and others are much larger (up to 10 cm in diameter) The neoplastic cells are demarcated from the adjacent parenchyma by a well-defined, intact capsule . These features are important in making the distinction from multinodular goitersAreas of hemorrhage, fibrosis, calcification, and cystic change, similar to those encountered in multinodular goitersare common in follicular adenomas
the constituent cells often form uniform-appearing follicles that contain colloid The follicular growth pattern within the adenoma is usually quite distinct from the adjacent non-neoplastic thyroid. This is another feature distinguishing adenomas from multinodular goiters, in which nodular and uninvolved thyroid parenchyma may have similar growth patterns. The epithelial cells composing the follicular adenoma reveal little variation in cell and nuclear morphology
the clinical presentation and behavior of a follicular adenoma with oxyphilia (Hürthle cell adenoma) is no different from that of a conventional adenoma. Other variants include extensive clear cell change of the cytoplasm (clear cell follicular adenoma) and "signet-ring" features (signet-ring cell follicular adenoma). careful examination of the tumor capsule to exclude capsular and/or vascular invasionThe hallmark of all follicular adenomas is the presence of an intact, well-formed capsule
encircling the tumor. Careful evaluation of the
integrity of the capsule is therefore critical
in distinguishing follicular adenomas from
follicular carcinomas, which demonstrate
capsular and/or vascular invasion
CARCINOMAS
accounting for about 1.5% of all cancers, Most cases occur in adults
? • Papillary carcinoma (75% to 85% of cases)
? • Follicular carcinoma (10% to 20% of cases)
? • Medullary carcinoma (5% of cases)
? • Anaplastic carcinoma (<5% of cases)