Posterior Pituitary Gland Pathology Study Guide

Cells of the Pituitary Gland
FOXO1 is present in the nuclei of pituitary cells at an increasing frequency as development progresses. Immunohistochemistry for FOXO1 (green) was performed on midsagittal pituitary sections. (A) FOXO1 is present in the developing pituitary by e10.5. Nuclear FOXO1 is apparent where the invaginating Rathke’s pouch is joined to the oral ectoderm that will form the mouth (see inset). (B) By e12.5 FOXO1 is present almost entirely in the cytoplasm of pituitary cells. (C) A few pituitary cells contain nuclear FOXO1 at e14.5. (D) At e18.5 the developing pituitary contains a mostly nuclear FOXO1. (E) In adults, FOXO1 is present in the anterior and intermediate lobes of the pituitary gland, but not in the posterior lobe (data not shown). In the adult pituitary FOXO1 is primarily nuclear (inset, arrow). Some cytoplasmic FOXO1 (inset, arrow head) is also present. (F) Immunohistochemistry for FOXO1. (G) Beta-galactosidase staining of pituitary from Foxo1+/LacZ mice identifies cells in which the endogenous Foxo1 promoter is active. (H) An overlay of immunohistochemical staining for FOXO1 (green) and β-galactosidase staining of pituitary from Foxo1+/LacZ mice (blue). (F–H) Arrows highlight examples of co-localized cells. Pictures are taken at 200X (A–E) or 630X (F–H). Insets are magnified 600X. Scale bars represent 100 µm. All cell nuclei were marked with DAPI (A–E, blue). Oral ectoderm (OE), infundibulum (INF), ventral diencephalon (VD), Rathke’s pouch (RP), posterior lobe (PL), intermediate lobe (IL), anterior lobe (AL). Forkhead Box O1 is present in quiescent pituitary cells during development and is increased in the absence of p27 Kip1: Majumdar S, Farris CL, Kabat BE, Jung DO, Ellsworth BS - PloS one (2012). Not altered. CC.

Posterior Pituitary Gland Pathology Video

Posterior Pituitary Gland

The hypothalamus produces oxytocin and antidiuretic hormone (ADH), which are subsequently sent by axons to the posterior pituitary for release.

The distal tubules and collecting ducts of the kidney are affected by antidiuretic hormone (ADH), which encourages free water retention.

The release of breast milk (let-down) in breastfeeding mothers and the contraction of the uterus during childbirth are both mediated by oxytocin.

Posterior gland pathology includes:

  • Central diabetes insipidus
  • Nephrogenic diabetes insipidus
  • Syndrome of inappropriate ADH secretion (SIADH)
  • Posterior Pituitary Gland
    Posterior Pituitary Gland. Pituitary gland illustration by Diberri. Not altered. CC BY-SA 3.0

Central Diabetes Insipidus

Central diabetes insipidus results from anti-diuretic hormone (ADH) deficiency.

Central diabetes insipidus occurs due to hypothalamic or posterior pituitary pathology such as:

  • Tumors
  • Trauma
  • Infections
  • Inflammation

Clinical characteristics of central diabetes insipidus include:

  • Polyuria
  • Polydipsia
  • Dehydration
  • Hypernatremia
  • Low urine osmolality and specific gravity

Central diabetes insipidus is diagnosed by failure of a water deprivation test to raise urine osmolality.

Central diabetes insipidus is treated with desmopressin (an antidiuretic hormone (ADH) analog).

  • Syndrome of Inappropriate ADH secretion
    Magnetic resonance imaging (MRI) and MR angiography findings. a, b Diffusion-weighted magnetic resonance imaging (DWI) showed the hyperintensity in the left dorsolateral medulla (a, white arrow) with hypointensity on apparent diffusion coefficient (ADC)-map (b, black arrow). c MR angiography demonstrated no obvious occlusion. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with lateral medullary syndrome: case report and literature review. Nakano H, Yanase D, Yamada M - BMC neurology (2016). Not Altered. CC.

Nephrogenic Diabetes Insipidus

Nephrogenic diabetes insipidus is due to impaired renal response to ADH.

Common causes of nephrogenic diabetes insipidus include:

  • Inherited mutations
  • Lithium
  • Demeclocycline

Desmopressin has little effect despite having clinical characteristics that are comparable to those of central diabetes insipidus.

  • Syndrome of Inappropriate ADH secretion
    Magnetic resonance imaging (MRI) and MR angiography findings. a, b Diffusion-weighted magnetic resonance imaging (DWI) showed the hyperintensity in the left dorsolateral medulla (a, white arrow) with hypointensity on apparent diffusion coefficient (ADC)-map (b, black arrow). c MR angiography demonstrated no obvious occlusion. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with lateral medullary syndrome: case report and literature review. Nakano H, Yanase D, Yamada M - BMC neurology (2016). Not Altered. CC.

Syndrome of Inappropriate ADH (SIADH) Secretion

Syndrome of inappropriate of ADH (SIADH) secretion is due to excessive ADH secretion.

Causes of syndrome of inappropriate of ADH (SIADH) secretion include:

  • Small cell lung cancer is most frequently brought on by ectopic production
  • Central nervous system injury
  • Pulmonary infection
  • Medications such as cyclophosphamide

Symptoms of syndrome of inappropriate of ADH (SIADH) secretion include:

  • Hyponatremia and low serum osmolality
  • Mental status changes
  • Seizures

Hyponatremia results in neuronal swelling and cerebral edema.

Treatment of syndrome of inappropriate of ADH (SIADH) secretion includes:

  • Free water restriction
  • Demeclocycline
  • Syndrome of Inappropriate ADH secretion
    Magnetic resonance imaging (MRI) and MR angiography findings. a, b Diffusion-weighted magnetic resonance imaging (DWI) showed the hyperintensity in the left dorsolateral medulla (a, white arrow) with hypointensity on apparent diffusion coefficient (ADC)-map (b, black arrow). c MR angiography demonstrated no obvious occlusion. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with lateral medullary syndrome: case report and literature review. Nakano H, Yanase D, Yamada M - BMC neurology (2016). Not Altered. CC.
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