Endocrine glands that produce increased amounts of hormone are considered hyperfunctional and may undergo hypertrophy (increase in the size of each cell) and hyperplasia (increase in the number of cells). The hyperfunction may be primary, caused by some abnormality within the gland itself, or secondary (compensatory), caused by changes in the serum concentration of a substance that normally regulates the hormone and may in turn be regulated by the hormone. For example, patients diagnosed with primary hyperplasia of the parathyroid glands have increased serum calcium concentrations as a direct result of an abnormality of the parathyroid glands. In contrast, patients diagnosed with secondary parathyroid hyperplasia have decreased serum calcium concentrations, resulting in stimulation of the parathyroid glands to produce more parathormone in an attempt to restore serum calcium concentrations to normal.

In some instances, some of the cells of a hyperplastic gland undergo a series of transformations that results in the formation of a tumour. In most instances, however, endocrine tumours arise from normal endocrine tissue. Endocrine tumours are largely autonomous, meaning that they are insensitive to any inhibition of hormone production imposed upon them through negative feedback control mechanisms. The vast majority of endocrine tumours are benign tumours (adenomas), but a few are malignant tumours (carcinomas). Malignant tumours are not only hyperfunctional but are also capable of invading adjacent structures and spreading (metastasizing) to distant organs. Some patients have tumours of several endocrine glands (see below Ectopic hormone and polyglandular disorders), which has been described as a hereditary syndrome called multiple endocrine neoplasia (MEN). While many endocrine tumours are hyperfunctional, others do not produce hormones at all.

Excess hormone secretion and the resultant symptoms may be caused by intrinsic endocrine gland hyperplasia or tumours or by abnormal stimulation. One example of abnormal stimulation that leads to endocrine hyperfunction is Graves disease, which is characterized by the production of antibodies that bind to and stimulate the receptors for thyrotropin in the thyroid gland. This results in the uncontrolled production of thyroid hormone and thyroid hyperplasia. Other syndromes of endocrine hyperfunction may result when a small endocrine tumour, innocuous in itself, secretes excessive amounts of a stimulatory hormone, which then causes secondary hyperplasia of the target gland. A classic example of such a situation is Cushing disease, in which a small pituitary tumour produces excess quantities of adrenocorticotropin that cause hyperfunction and hyperplasia of the adrenal glands.

Some endocrine tumours produce excess quantities of the expected hormone and excess amounts of a hormone that is normally secreted by a different endocrine gland. For example, medullary carcinomas of the thyroid originate from C cells (parafollicular cells) that normally produce calcitonin, a hormone that transiently decreases serum calcium concentrations. These tumours may produce not only calcitonin but also adrenocorticotropin, which is normally secreted by cells of the pituitary gland. In addition, tumours arising from tissues that ordinarily have no endocrine function may produce one or more hormones. A typical example is lung cancer, which may produce one or more of an array of hormones, most commonly vasopressin (antidiuretic hormone) and adrenocorticotropin. Such tumours are called ectopic hormone-producing tumours.