May be sporadic, endemic (in areas of iodine-deficiency), or, rarely, familial.

Majority of patients are euthyroid and asymptomatic; a slow, gradual (10–20 % per year) increase in volume is usual.

Pathological variants include Hürthle cell adenoma, hyalinizing trabecular adenoma, and atypical follicular adenoma.

Since follicular adenomas cannot be differentiated from carcinomas using fine needle aspiration biopsy (FNAB), the term “follicular neoplasm” is used, and surgical excision is required to establish a definite diagnosis.

They may be caused by a variety of etiologies (infectious, inflammatory, degenerative, neoplastic), although cystic degeneration within a multinodular goiter is the most common cause.

Clinical findings include the presence of a diffuse goiter, signs of hyperthyroidism (tachycardia, tremor, arrhythmia), and, in a minority, signs of ophthalmopathy.

Thyroid eye disease and pretibial myxedema differentiate Graves’ disease from other causes of hyperthyroidism.

Hashimoto’s thyroiditis may after many years progress to hypothyroidism and FNABs are characterized by lymphocytic infiltration and associated Hürthle cell metaplasia.

Thyroid lymphoma may very rarely develop in goiters affected by Hashimoto’s thyroiditis.

Usually self-limiting over weeks and managed symptomatically.

This results in permanent hypothyroidism in around 50 % of affected women.

The cause is unknown, but it may be associated with other similar inflammatory sclerosing conditions such as retroperitoneal fibrosis or fibrous mediastinitis.

They are due to persistence of the stalk of epithelial cells that descend down from the floor of the primitive pharynx during development of the thyroid. The stalk normally undergoes atrophy at 6 weeks, but its persistence leads to cyst formation.