Parathyroids – usually 4 parathyroid glands (some people may have five or six)

• Congenital and Developmental Abnormalities – abnormalities in migration the glands from embryonic origin in the branchial pouches Þ ectopic parathyroids
• lower glands tend to be more widely distributed (may be found in thymus, mediastinum, carotid bifurcation, pericardium)
• Parathyroid hyperplasia: hyperplasia typically involves ALL 4 glands. Unknown etiology. Treatment: resection of 3.5 glands
• Parathyroid adenoma: Adenoma is usually SOLITARY. Treatment: debridement of involved gland
• Parathyroid carcinoma: Uncommon. Evident lesion by gross tumor invasion or distant metastasis. Treatment: Wide resection.

• Accessory and Heterotopic Adrenal Tissue: Recall that the adrenal tissue (mesodermal mesenchyme and neuroectodermal cells) migrate along with gonadal tissue during embryonic development – adrenal tissue may therefore be found anywhere along the line of gonadal descent (celiac axis is also a common site)
• tissue may contain cortex and medulla or cortex only
• Adrenal cortical insufficiency:
• Primary (or Autoimmune) Addison’s Disease – autoimmune or idiopathic destruction of adrenal tissue
• symptoms do not develop until more than 90% of tissue is destroyed
• Histology – intense lymphocyte infiltrate and plasma cells within gland, parenchymal destruction and atrophy due to autolysis; thinned and discontinuous cortex. Microscopic appearance similar to Hashimoto’s Thyroiditis.
• Secondary Adrenal Cortical Insuffiency – destruction of pituitary gland Þ lack of ACTH Þ Addison symptoms
• Histology – very atrophic (marked reduction in adrenal cortical mass due to lack of ACTH)
• Infectious Diseases – tuberculosis, fungal infection (histoplasmosis blastomycosis, coccidiodomycosis, cryptococcus), viruses (herpes, CMV, varicella zoster)
• Histology – extensive caseating necrosis, granuloma formation
• Waterhouse-Friderichsen Syndrome: associated with Neisseria meningitidis, Strep species and Hemophilus influenzae
• Mechanism – infection Þ septic shock Þ disseminated intravascular coagulation Þ hemorrhage in adrenal glands
• Metastatic tumors – 13-27% of cancers develop metastases; usually from lung, breast, or melanoma
• Adrenal Cortical Hyperplasia – associated with hyperfunction of adrenal glands
• hyperplasia due to ACTH excess either from pituitary-derived ACTH (Cushing’s disease) or ectopic ACTH secretion
• Conn’s syndrome – adrenal cortical hyperplasia with hyperaldosteronism
• Adrenal Neoplasm – can occur in cortex or medulla
• Cortex – adenoma (benign) or carcinoma (malignant)
• endocrine hyperfunction resulting from a neoplasm that secretes excessive cortisol
• Histology – clear, foamy or eosinophilic cytoplasm occupying the gland with atrophy of residual cortex.
• Medulla – pheochromocytoma – surgically correctable form of hypertension
• uncommon neoplasm composed of chromaffin cells that syntesize and release large amounts of catecholamines

• Hypopituitarism – severe cases do not manifest until 90-98% of tissue is lost. Causes:
• ischemic necrosis (head trauma, CVA, post-partum hemorrhage (Sheehan’s syndrome)
• transection of pituitary stalk, embolism, thrombosis, DIC, and vasospasm
• infarction of posterior pituitary leading to diabetes insipidus
• Pituitary Neoplasms
• Pituitary adenoma – 2 mechanisms for symptoms
• (1) compression on adjacent anatomic structures (cranial nerve disturbances, headaches, intercranial pressure)
• (2) endocrine hypo- or hyperfunction
• Craniopharyngionoma – tumor derived from the vestigal remnants of Rathke’s pouch (stomodermal ectoderm-oral)
• Histology – cystic or sold; nests and cords of stratified squamous or columnar epithelium; 75% contain calcifications

• Group of inherited disorders characterized by development of hyperplastic and neoplastic lesions of endocrine organs
• MEN Type I (Werner Syndrome) – chromosomal abnormality on chromosome 11q13
• can be familial or sporadic; familial form is autosomal dominant with high penetrance
• abnormalities involving the parathyroids, pancreas, and pituitary glands (the 3P’s)
• MEN Type II: chromosomal abnormality near centromeric region of chromosome 10
• autosomal dominant with variable penetrance
• MEN Type IIA (Sipple Syndrome)-medullary thyroid carcinoma (100%), parathyroid hyperplasia, pheochromocytoma
• MEN Type IIB or III – medullary thyroid carcinoma, phyeochromocytoma, and multiple neuromas involving conjunctiva, buccal mucosa, tongue, lip, and GI tract
• Familial Medullary Thyroid Cancer (FMTC) – chromosome 10; autosomal dominant with high penetrance