Goiters

• Goiter or enlargement of the thyroid is the most common manifestation of thyroid disease
• Diffuse and multinodular goiters reflect impaired synthesis of thyroid hormone, most often causes by dietary iodine deficiency
• The compensatory increase in TSH causes hypertrophy and hyperplasia of the thyroid follicular cells causing gross enlargement of the thyroid gland
• In the majority of people the compensatory increased thyroid mass is able to overcome the hormone deficiency, resulting in a euthyroid state
• If the underlying defect is too severe to be overcome the impaired hormone production it will result in a goitrous hypothyroidism
• The degree of thyroid enlargement is proportional to the level and duration of hormone deficiency

 

Diffuse Nontoxic (Simple) Goitre

• No nodularlity
• May be endemic or sporadic
• Endemic goitres result when there is dietary iodine deficiency. It occurs in the Alps, Andes and Himalayas. In addition is certain areas there are dietary substances called goitrogens which interfere with thyroid function worsening any condition due to iodine deficiency. Goitrogens include excessive calcium and vegetables such as cabbage, turnip, cauliflower, Brussels sprouts and cassava root
• Sporadic goitre occurs less frequently and is most commonly seen in young girls. It can be caused by a number of conditions which affect thyroid hormone synthesis. It may be due to hereditary enzyme defects that are transmitted in an autosomal recessive manner. In most cases the cause is not known

 

Morphology

• Two phases can be identified in the evolution of diffuse non-toxic goiter;
• The hyperplastic phase
• Phase of colloid involution
• The hyperplastic phase the thyroid gland is diffusely and symmetrically enlarged. The follicules are lined with crowded columnar cells
• If dietary iodine subsequently increases or the demand for thyroid hormone decreases, the stimulated follicular epithelium involutes to form an enlarged, colloid rich gland called a colloid goitre

 

Clinical course

• Vast majority of patients are clinically euthyroid
• TSH levels are normally elevated

 

Multinodular goiter

• Due to recurrent episodes of hyperplasia and involution resulting in a more irregular enlargement of the thyroid
• Virtually all log standing simple goiters develop into multinodular goiters
• May be non-toxic or produce thyrotoxicosis
• May be mistaken for carcinomas
• Because they are derived from simple goiters they show the same endemic and sporadic patterns and female preponderance
• May be due to variations among follicular cells to respond to external stimuli
• The uneven follicular hyperplasia, uneven accumulation of colloid and various tensions and stresses can lead to haemorrhages, scarring and calcifications
• The scarring adds to the tension resulting in more nodularity

 

Morphology

• Multilobular, asymmetrically enlarged glands which may reach a weight of 2000g
• One lobe may be more affected than the other resulting in lateral pressure on midline structures such as the trachea and the oesophagus
• The goiter may grow between the sternum and the clavicles to produce the intrathoracic or plugging goitre
• Regressive changes occur frequently particularly in older lesions resulting in areas of haemorrhage, fibrosis, calcification and cystic change
• Microscopic appearance includes colloid rich follicles lined by flattened inactive epithelium and areas of follicular epithelial hypertrophy and hyperplasia

 

Clinical course

• Dominant effect is due to the mass effect of the enlarged gland
• May cause airway obstruction, dysphagia and compression of the large vessels of the neck and upper thorax
• Most people are euthyroid but in a minority a hyperfunctioning nodule may develop resulting in hyperthyroidism
• Radioionine uptake is uneven with hyperfunctioning nodules concentrating the iodine and appearing ‘hot’

May mask or