Endocrine System

Published on 19/03/2015 by admin

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Endocrine System

The endocrine system consists of a number of organized glands, groups of cells, and dispersed solitary cells that control the functional balance of internal organs by means of chemical messengers called hormones. Organized endocrine glands include the pituitary, the thyroid and parathyroid, the adrenal cortex and medulla, and the endocrine pancreas. In addition, sex organs such as the ovary and testis produce certain hormones (see chapters 7 and 8).

Thyroid Gland

The thyroid gland, which responds with peripheral feedback control to the hypothalamus and pituitary, is the key endocrine organ controlling energy metabolism (carbohydrate and lipid catabolism, stimulation of protein synthesis). It acts primarily through the effects of 2 hormones, thyroxin (tetraiodothyronine; T4) and triiodothyronine (T3), which bind to receptors on various peripheral cells and stimulate their metabolic activities. These hormones are coupled to thyroglobulin and are stored in follicular colloids. Proteolytic enzymes release T4 and T3 and make it available in the periphery as active hormones. This process is accompanied morphologically by signs of follicular activation such as paraepithelial resorptive vacuoles in the colloid, epithelial swelling (cuboidal size), and proliferation (focal stratification to form Sanderson cushions and papillae).

Parathyroid Glands

In most people, 4 separate parathyroid glands lie in close proximity to the posterior part of the thyroid gland. Their hormone, parathyroid hormone (PTH), controls the calcium balance of the body as it responds to feedback mechanisms independently of hypothalamic-hypophysial supervision. One third of the normal parathyroid gland consists of fat tissue, and the balance contains the pale PTH-producing chief cells and pink oxyphilic cells. Any increase in weight above the normal 130 mg or replacement of fat tissue by glandular cells indicates hyperplasia/hyperfunction. Hyperparathyroidism independent of feedback control (i.e., autonomous) usually is caused by adenomas or carcinomas of the gland. Hypoparathyroidism (lack of PTH) is rare, usually follows surgical resection of the glands in thyroidectomies, and causes severe hypocalcemia. Familial autosomal recessive forms of hypoparathyroidism may occasionally occur as part of a multiglandular deficiency or in combination with T-cell immune deficiency (e.g., DiGeorge syndrome). The ionized serum calcium level provides the stimulus for PTH secretion. PTH stabilizes the serum calcium level by inhibiting renal tubular phosphate reabsorption and calcium/phosphate absorption in the bone and by enhancing calcium absorption in the intestines.

Adrenal Cortex (Suprarenal Cortex)

The adrenal cortex is composed of 3 microscopically identifiable zones, each of which engages in the production of different hormones: the zona glomerulosa (outer zone), the zona fasciculata (intermediate zone), and the zona reticularis (inner zone adjacent to adrenal medulla). The latter 2 zones respond to stimulation by hypophyseal corticotropin, whereas the zona glomerulosa functions independently of it. This zone produces the hormone aldosterone in response to increases in potassium levels and angiotensin or decreases in atrial natriuretic peptide or somatostatin. The 2 inner zones produce glucocorticoids and androgens in response to corticotropins. Increased functional activity in either zone is associated with microscopic hyperplasia, adenoma, or carcinoma; decreased functional activity is associated with atrophy (e.g., in malnutrition), necrosis (e.g., in septicemia, tuberculosis, or viral infection), or autoimmune adrenalitis.

Adrenal Medulla

The major organs of the sympathetic neuroendocrine system are the adrenal medulla and less compact collections of neuroendocrine cells in paraganglia, including the carotid body and the organ of Zuckerkandl. All consist of chromaffin cells (which have an affinity to chromium salts and stain dark on oxidation), which produce the catecholamines epinephrine and norepinephrine. Several tumors of chromaffin catecholamine-producing cells, such as pheochromocytoma and paragangliomas, exaggerate the physiologic functions of the organs. In addition, ganglionic cells in these regions may give rise to neuroblastomas. Approximately 10% of pheochromocytomas are part of a familial syndrome called multiple endocrine neoplasia (MEN). Several forms of MEN are autosomal dominant diseases with mutations on chromosomes 10 and 11. Patients with an identified adenoma or carcinoma at one of these organ sites and their families must therefore be screened for other endocrine abnormalities.

Endocrine Pancreas

The endocrine pancreas consists of the islets of Langerhans. These are composite fabrication sites composed of different cells that produce and secrete several hormones. The greatest proportion (60-70%) are insulin-producing β cells; α cells (15–20%) produce the “insulin antagonist” glucagon. There are several clones of δ cells (e.g., D cells, D1 cells) which secrete somatostatin or vasoactive intestinal polypeptide (VIP) as well as cells that produce substance P, human pancreatic polypeptide, or gastrin (G cells). Consequently, pancreatic endocrine adenomas or carcinomas (e.g., gastrinoma, vasoactive intestinal polypeptide–secreting tumor [VIPoma], somatostatinoma, and others) can affect multiple endocrine activities. This chapter focuses only on the more common types of hyperinsulinism and hypoinsulinism (diabetes mellitus).

TABLE 12-1


Entity Pathology Pathogenesis
Lymphofollicular thyroiditis (Hashimoto thyroiditis), chronic Lymphocytic/plasmacellular infiltrate with lymph follicles, follicle destruction, oxyphilic metaplasia of follicle cells (Hürthle or Askanazy cells) T-cell autoimmune reaction (TPO, TMA), genetic predisposition
Granulomatous thyroiditis (de Quervain thyroiditis), subacute Microfocal neutrophilic infiltrates, follicle destruction with secondary giant cell granulomatous reaction, marked lymphoplasmacellular infiltrates E.g., virus infection: coxsackie, adenovirus, mumps, and others, secondarily autoimmune
Chronic sclerosing thyroiditis (Riedel thyroiditis) Lymphocytic thyroiditis with progressive glandular atrophy and fibrosis extending to adjacent tissues Suggestively autoimmune*
Painless subacute thyroiditis Lymphocytic infiltrates with eventual follicular destruction, usually self-limited, hyperthyroid Unknown HLA-DR3 associated

TMA indicates thyroid microsomal antigen; TPO, thyroid peroxidase antigen.

*Associated with primary sclerosing cholangitis

TABLE 12-2


Carcinoma Frequency* Pathology and Spread Prognosis
Papillary carcinoma Approximately 80% Solitary or multifocal lesions with papillary structures and ground glass “empty” nuclei; preferentially lymphatic spread 10-year survival 90% (in younger persons)
Follicular carcinoma Approximately 15% Infiltrative follicular structures without ground glass nuclei; preferentially hematogenous spread 10-year survival 85% (early cancer); 45% in invasive form
Medullary carcinoma originate from C cells Up to 5% Solitary or multifocal lesions with pale round or spindle cells and stromal amyloid deposits; hematogenous and lymphatic spread 5-year survival <10%
Anaplastic carcinoma Rare Highly anaplastic pleomorphic with giant cells or spindle cells, sarcomatous appearance; rapid hematogenous metastases 5-year survival <10%


*Percentage of all thyroid carcinomas.

Prognosis under optimal conditions of early detection.

MEN type II (IIa) Sipple syndrome MEN type III (IIb) Mucosal neuroma syndrome


MEN indicates multiple endocrine neoplasia.

*With some selectivity in individual patients.

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