Adrenocorticotropic Hormone 003

Adrenocorticotropic Hormone 003

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Pituitary tumors are

common neoplasms, and recognition of their presentation is critical since a favorable therapeutic outcome is dependent on early identification of the lesion.

Multiple oncogene abnormalities may be involved in pituitary tumorigenesis. Glycoprotein abnormalities, gene mutations, p53 gene deletions, mutations, and rearrangements, and association of pituitary tumors with the syndrome of multiple endocrine neoplasia have been described and are involved in the development of adenomas in the pituitary gland. The pituitary tumor transforming gene-1 (PTTG-1) is a newly discovered oncogene that serves as a marker of malignancy grades in several endocrine malignancies; this gene is known to regulate the cellular mitosis process and forced expression of this gene induces tumor formation in mice. PTTG-1 is overexpressed in pituitary tumors.⁽⁴⁸⁾ most of these tumors are benign, but certain factors involved in the genesis of  the tumor may determine its rate of growth and aggressiveness. For instance, the presence of p53 gene correlates with more 

aggressive tumor behavior

Clinical manifestations are due to the local effect of the mass and distant endocrine manifestations that can affect a variety of organ systems. These effects are due to lack or excess of a given stimulating hormone on the targe. Pituitary adenomas, with a few exceptions, are not under the control of hypothalamic releasing factors⁽⁴⁸⁾ .

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Gonadotropins (FSH and LH) 002

Gonadotropins (FSH and LH) 002

إضافة تسمية توضيحية

The posterior pituitary is an extension of the hypothalamus and contains the axon terminals of magnocellular neurons located in the Supraoptic and paraventricular nuclei. These neurons generate and propagate action potentials, producing membrane depolarization and exocytosis of the contents of their secretory granules. The neuropeptides oduced by the magnocellular neurons, and consequently released from posterior pituitary, are oxytocin and arginine vasopressin

1.    Oxytocin :

The neuropeptide oxytocin is synthesized by magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus and is released from the posterior pituitary into the peripheral circulation. The release of oxytocin is stimulated during breast-feeding (lactation) and childbirth (parturition)⁽⁴²⁾.

The two main target

 organs for oxytocin's physiologic effects are the lactating breast and the uterus during pregnancy. In the lactating breast, oxytocin stimulates milk ejection by producing contraction of the myoepithelial cells that line the alveoli and ducts in the mammary gland. In the pregnant uterus, oxytocin produces rhythmic contractions to help induce labor and to promote regression of the uterus following delivery. Oxytocin is used clinically during labor and delivery to promote uterine contractions and during the postpartum period to help decrease bleeding and return the uterus to its normal size (uterine involution) ⁽⁴²⁾.

2.    Arginine Vasopressin (AVP)

Arginine vasopressin, also known as antidiuretic hormone (ADH),  the other neuropeptide produced by magnocellular neurons of the hypothalamus and released from the posterior pituitary. The principal effect of AVP is to increase water reabsorption by enhancing permeability to water in the distal convoluted tubules and the medullary collecting ducts in the kidney. The result is the production of smaller volumes of concentrated urine. In addition, AVP increases vascular resistance. This function of AVP may be important during periods of severe lack of responsiveness to other vasoconstrictors, as may occur during severe blood loss (hemorrhagic shock) or systemic infection  (sepsis)⁽⁴³⁾.

The importance of AVP is better understood in terms of the total amount of urine that would be. excreted in its absence. For example, in a healthy individual an average of 180 L of glomerular filtrate is formed per day. Thus, without AVP-mediated reabsorption of 10% of filtered water in the distal collecting ducts, urine output would be close to 18 L/d. This is 10-fold higher than the volume of urine output (1.5-2 L/d) under  normal conditions⁽⁴³⁾. 

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Phyisology of the Pituitary Gland 001

Phyisology of the Pituitary Gland 001

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FIRST HORMONES OF THE ANTERIOR PITUITARY GLAND

The anterior pituitary, or adenohypophysis, plays a central role in the regulation of endocrine function through the tropic hormones. The production of tropic hormones, is under hypothalamic regulation by the hypophysiotropic neuropeptides released in the median eminence The tropic hormones produced by the anterior pituitary are released into the systemic circulation, from where they reach their target organs to produce a physiologic response, most frequently involving the release of a target organ hormone. The hormones produced by the target organs affect anterior pituitary function as well as the release of hypophysiotropic neuropeptides, maintaining an integrated feedback control system of endocrine function⁽³⁸⁾.

The hormones of the anterior pituitary can be classified into 3 families: the glycoproteins, those derived from proopiomelanocortin (POMC), and those belonging to the GH and prolactin family.

I- Glycoproteins:

They include TSH, FSH, LH, and human chorionic gonadotropin produced by the placenta. These hormones are heterodimeric glycoproteins consisting of a common subunit and a unique subunit, which confers the biologic specificity of each hormone.

1.      Thyroid-Stimulating Hormone :

TSH is a glycoprotein synthesized and secreted from thyrotrophs of the anterior pituitary gland.. They synthesize and release TSH in response to thyrotropin-releasing hormone (TRH) stimulation. TRH is synthesized in the paraventricular nuclei of the hypothalamus,. TRH binds to a protein-coupled receptor, which· activates phospholipase C, leading to increased phosphoinositide turnover, calcium mobilization, formation of cyclic adenosine monophosphate (cAMP), and release of TSH into the circulation. TSH binds to a protein-coupled receptor in the thyroid gland, activating adenylate cyclase, which leads to increased intracellular cAMP formation. TSH stimulates all the events involved in thyroid hormone synthesis and release. In addition, it acts as a growth and survival factor for the thyroid gland. The release of TSH from the anterior pituitary gland is under negative feedback inhibition by thyroid hormone.       

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