Reporter and Curator: Dr. Sudipta Saha, Ph.D.
- Multiple important and complex interactions exist between the endocrine and other systems (e.g. immune, nervous).
- Definition of hormones: circulating molecules with a site of action distant from site of origin with ability to bind to cellular receptors and initiate signal transduction via conformational changes in the receptor.
- Hormones participate in growth and development, reproduction, energy metabolism and maintenance of the internal environment.
- In general, hormones are protein-derived molecules that bind to cell surface receptors or steroid hormones that bind to nuclear receptors. An exemption is thyroid hormone, a modified amino acid that binds to nuclear receptors.
- Integrated feedback loops are very characteristic to the endocrine system and critical in maintaining normal hormonal function. Two major types of control exist: the hypothalamic-pituitary-peripheral organ unit and the free standing endocrine gland.
- Pathology in endocrinology is due to abnormal hormone activity or neoplasms, leading to endocrine hyperfunction/hyperfunction or structural abnormalities.
Endocrine pathology is derived from defects found at any point in the hormonal synthesis, secretion, transport, action, or regulatory control of a hormone. Endocrine pathology often occurs in one of the following broad categories:
- Abnormal Hormone Activity which can be subdivided into:
- Endocrine organ hypofunction
- Primary endocrine organ failure can be genetic or acquired
- Endocrine organ agenesis (absence)
- Genetic defect in hormone biosynthetic pathway (e.g. adrenal insufficiency due to 21-hydroxylase deficiency)
- Destruction due to
- Autoimmune disease (e.g. Hashimoto’s hypothyroidism)
- A tumor, infection or hemorrhage
- Deficiency of precursor (e.g. iodine deficiency leading to decreased thyroid hormone synthesis)
- Production of abnormal hormone resulting in hypofunction (e.g. abnormal glycosylation of TSH). Secondary endocrine organ failure (e.g. hypothyroidism due to hypopituitarism)
- Primary endocrine organ failure can be genetic or acquired
- Endocrine organ hyperfunction
- Primary endocrine organ process due to a benign condition (e.g. autoimmune thyroid gland stimulation in Graves’ disease) or benign neoplasm (e.g. primary hyperparathyroidism causing hypercalcemia). Endocrine cancers are rare but they may also release hormones that cause endocrine hyperfunction (e.g. adrenocortical carcinoma secreting excessive androgens causing virilization).
- Benign condition (e.g. thyroid gland stimulation in Graves’ disease by autoantibodies against the TSH receptor)
- Benign neoplasm (e.g. primary hyperparathyroid adenoma secreting excessive PTH causing hypercalcemia).
- Endocrine cancers (e.g. adrenocortical carcinoma secreting excessive androgens causing virilization).
- Secondary due to stimulation by a trophic/stimulatory hormone, most often due to a benign neoplasm (e.g. hypersecretion of cortisol from adrenal cortex due to and ACTH-secreting pituitary adenoma).
- Less commonly, ectopic production of a hormone may lead to endocrine hyperfunction (e.g. ACTH released from small cell lung cancer cause hypersecretion of cortisol by adrenal glands).
- Primary endocrine organ process due to a benign condition (e.g. autoimmune thyroid gland stimulation in Graves’ disease) or benign neoplasm (e.g. primary hyperparathyroidism causing hypercalcemia). Endocrine cancers are rare but they may also release hormones that cause endocrine hyperfunction (e.g. adrenocortical carcinoma secreting excessive androgens causing virilization).
- Abnormality in hormone transport or metabolism (e.g. genetic defects of abnormal thyroid binding globulin)
- Abnormal hormone receptor binding and/or signal transduction. Most often causing endocrine hypofunction due to resistance to the action of hormone. The receptor itself being unable to bind the hormone (e.g. thyroid hormone resistance) or there may be a defect in post-receptor signal transduction (e.g. type 2 diabetes mellitus). Occasionally, abnormal hormone signaling may lead to endocrine hyperfunction (e.g. Gs protein mutation leading to unregulated secretion of Growth Hormone).
- Endocrine organ hypofunction
- Neoplasms. They can be both benign or malignant. Symptoms develop either due to
- Overproduction of hormone by the tumor (e.g. ACTH producing pituitary adenoma causing hypersecretion of cortisol)
- Underproduction of nearby hormones due to mass effect (e.g. pituitary hormone production is often affected by large pituitary tumors)
- Structural damage (e.g. hypothalamic-pituitary tumors causing headache, visual problems).
- Iatrogenic. Most common iatrogenic cause of endocrine abnormality is exogenous administration of glucocorticoids (give to treat non-endocrine conditions, e.g. rheumatoid arthritis)
Source References:
http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/
http://ocw.tufts.edu/Content/14/lecturenotes/265876
Greenspan FS and Gardner DG. Basic and Clinical Endocrinology, 6th edition. Lange Medical Books, McGraw-Hill, 2001.
Wilson, JD, Foster, DW, Kronenberg, HM, and Larsen, PR. Principles of Endocrinology. In: Williams Textbook of Endocrinology, 9th edition, W.B. Saunders, Philadelphia, 1998.
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