Disorders Of Anterior Pituitary Gland

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AnatomyThe pituitary has two parts, an anterior lobe and a posterior lobe. Each lobe releases different hormones. The pituitary gland is attached to the bottom of the hypothalamus, a part of the brain that connects the nervous system and endocrine system. The hypothalamus releases hormones, and it signals the pituitary gland to release hormones.

Rare disorders: Many pituitary disorders are uncommon. At the same time, estimates for the number of people with acromegaly or Cushing disease/syndrome may be too low. Estimates include:

The pituitary gland is an important part of the endocrine system. It communicates with many different parts of the endocrine system. Aside from the pituitary gland, the endocrine system contains the following glands and organs:

The pituitary gland is divided into two parts: the anterior pituitary and the posterior pituitary. Each part has its own job. The anterior pituitary makes and releases its own hormones, while the posterior pituitary stores and releases hormones that are made in the hypothalamus.

Essentially, if the hypothalamus is the commander of the endocrine system, the pituitary is the second-in-command. It receives instructions from the hypothalamus and sends those instructions out to the rest of the endocrine system.

Multiple disorders can affect your anterior pituitary gland. Most of these disorders are caused by physical damage. Other conditions that can cause poor anterior pituitary function include blood loss, infection, genetic conditions, and tumors.

In those assigned female at birth, Cushing disease may cause a thickening of body and facial hair and irregular or missing periods. In those assigned male at birth, it may cause erectile dysfunction and decreased fertility and sex drive.

Hyperthyroidism. Hyperthyroidism may occur when your pituitary gland releases too much thyroid-stimulating hormone, leading to an overactive thyroid. Symptoms of hyperthyroidism include:

The pituitary gland is in the brain and controls the functions of all the other endocrine glands. The pituitary gland itself is controlled by a nearby area called the hypothalamus. The pituitary gland is important for the health, growth and development of your child or teenager.

Diabetes insipidus results from insufficient production of ADH, a hormone that helps the body conserve the optimal amount of water. Diabetes insipidus is not related to diabetes mellitus, although some of the symptoms are similar.

Empty sella syndrome is characterized by an enlarged bony structure that houses the pituitary gland at the base of the brain. Symptoms, if they are present, can include impotence, reduced sexual desire and irregular menstruation.

Hypopituitarism, also called an underactive pituitary gland, affects the function of the anterior lobe of the pituitary gland. Hypopituitarism can have impact on hormone production in the adrenals, thyroid, testes or ovaries.

Most pituitary tumors are benign. However, because of the location of the pituitary gland, large pituitary tumors can press against the optic nerves, causing vision problems. In addition, pituitary tumors that produce excessive amounts of hormones overstimulate other endocrine glands and cause symptoms.

The most common hormone produced by pituitary tumors is prolactin. Prolactin-producing tumors (prolactinomas) are more frequent in women. They can cause irregularity or loss of periods, infertility and breast milk secretion. In men, excessive prolactin can cause reduced libido and erectile dysfunction.

Sheehan syndrome which is also called post-partum pituitary necrosis refers to the necrosis of cells of the anterior pituitary gland following significant post-partum bleeding, hypovolemia, and shock. Advances in obstetrical care in developed countries have reduced the incidence of this condition. However, it is still a significant cause of morbidity and mortality in less developed countries. This activity reviews the evaluation and management of Sheehan syndrome and discusses the role of interprofessional team members in collaborating to provide care and enhance patient outcomes.

Objectives:Identify the etiology of Sheehan syndrome conditions.Discuss the typical history and physical findings expected in Sheehan syndrome.Outline the management options available for Sheehan syndrome.Discuss interprofessional team strategies for improving care coordination and communication to identify Sheehan syndrome and improve outcomes.Access free multiple choice questions on this topic.

Sheehan syndrome which is also called post-partum pituitary necrosis refers to the necrosis of cells of the anterior pituitary gland following significant post-partum bleeding, hypovolemia, and shock. Advances in obstetrical care in developed countries have reduced the incidence of this condition. However, it is still a significant cause of morbidity and mortality in less developed countries. British pathologist Harold Leeming Sheehan first described this disorder in 1937.[1]

Sheehan syndrome occurs when the anterior pituitary gland is damaged due to significant blood loss. Classically, this happens after delivery, in which the mother loses a significant amount of blood. This blood loss results in the pituitary gland not being able to produce hormones. The diagnosis of Sheehan syndrome is not always apparent immediately after childbirth. Occasionally, the signs and symptoms of Sheehan syndrome may not present until months after childbirth or significant trauma. The first and most common symptom of Sheehan syndrome is the absence of lactation, also known as agalactorrhea. Other symptoms are associated with loss of pituitary gland hormone production and may include amenorrhea or oligomenorrhea, hot flashes, and/or decreased sex drive. Symptoms of hypothyroidism such as fatigue, bradycardia, hypotension, weight gain, and constipation may occur months later, along with the loss of axillary and pubic hair. Adrenal insufficiency can also occur with symptoms of fatigue and weight loss. Laboratory values that may support secondary adrenal insufficiency due to Sheehan syndrome could include hyponatremia, anemia, and hypoglycemia.[2][3]

Sheehan syndrome is rare in developed countries because of advanced obstetrical practices and more exposure to experienced medical providers and medical facilities. Unfortunately, it can be a complication of childbirth in developing and low-income countries. Some studies have placed the incidence of Sheehan syndrome as high as five patients out of 100,000 births.[1]

An increase in pituitary volume and cell count occur in pregnant women in the weeks preceding delivery. This increase is caused principally by hyperplasia of prolactin-producing cells (lactotrophs) and hyperplasia of other cells in the anterior pituitary gland. This hyperplasia leads to increased nutritional and metabolic demand by the anterior pituitary gland as a whole, but the blood supply that feeds the anterior pituitary does not increase. The blood supply that feeds the anterior pituitary gland is a relatively low-pressure system. It is theorized that this is the mechanism that makes the pituitary cells more susceptible to ischemia. Consequently, the cells of the anterior pituitary are more prone to necrosis in pregnancies complicated by significant postpartum hemorrhage. The posterior pituitary gland has its blood supply which functions under higher pressure than the anterior pituitary, so it is not usually affected by shock or hypovolemia.[4]

Sheehan syndrome is the clinical manifestation of anterior pituitary cell necrosis and may present as pan-hypopituitarism or as selective loss of pituitary function. Pan-hypopituitarism is a result when many cells of the pituitary are affected, as opposed to only a few cells. It is far more common than the selective loss of pituitary function. Prolactin and growth hormone are the most common hormones affected by selective pituitary necrosis and hypofunction. The posterior pituitary function is usually not affected, as stated above. However, diabetes insipidus can occur, but it is a rare manifestation of Sheehan syndrome.[5]

Patients may present with an acute or chronic presentation of Sheehan syndrome. The chronic condition of Sheehan syndrome is more common than the acute presentation. Confounding the presentation is that Sheehan syndrome may present months to years after the initial event of hypovolemia and shock.[2]

The acute presenting condition of Sheehan syndrome is usually evident when the mother of the newborn has difficulty with breastfeeding or cannot produce milk at all (agalactorrhea).[6] However, many women are asymptomatic for months to years after childbirth. Women may report difficulties with menses after childbirth, and some may never have menses until Sheehan syndrome is diagnosed and treated. The acute form of Sheehan syndrome can be quite dangerous if not recognized and treated quickly after childbirth. The persistent hypotension and tachycardia can mimic hypovolemia and shock, but hyponatremia and persistent hypoglycemia can help to clinch the diagnosis of Sheehan syndrome.[1]

Chronic Sheehan syndrome is diagnosed due to symptoms that occur due to hypopituitarism, and again, it can occur months to years after the initial vascular insult to the pituitary gland. Symptoms of hypothyroidism may occur months after childbirth. The patient may complain of fatigue, asthenia or weakness, hair loss, constipation, weight gain, problems with focusing or with their attention span, and cold intolerance. Physicians may note hypotension and bradycardia during the physical exam. Patients may also exhibit a secondary adrenal insufficiency which could have symptoms of fatigue and weight loss.[7] Lab values may reflect hypoglycemia, hyponatremia, and/or anemia.

Evaluation of anterior pituitary function is done by obtaining blood when a high clinical suspicion is evident to diagnose Sheehan syndrome. The hormones that are manufactured in the anterior pituitary gland are the gonadotropins such as follicle-stimulating hormone (FSH) and luteinizing hormone (LH), growth hormone (GH), prolactin (PRL), adrenocorticotropic hormone (ACTH), and thyroid-stimulating hormone (TSH). They are affected primarily in a certain order when necrosis occurs, GH first, followed by PRL, FSH, LH, ACTH, and then TSH last.[1] Laboratory tests to order would include a complete blood count (CBC) with differential count, basic metabolic profile, thyroid function tests (TSH, FT3, FT4), FSH, LH, prolactin, estrogen, cortisol, and growth hormone.[8] Finding a low basal hormone level along with a history and physical suggestive of Sheehan syndrome would help to make the diagnosis. Other laboratory tests that may occur with Sheehan syndrome include normocytic/normochromic anemia, thrombocytopenia, and/or pancytopenia. Hyponatremia and hypoglycemia may also be present as well. Other less common laboratory tests in the workup for Sheehan syndrome that may be abnormal include multiple thrombophilic genetic mutations, low PT and aPTT tests, anti-pituitary antibodies, and anti-hypothalamus antibodies.[9] These tests may be considered after the primary tests to confirm the diagnosis. Also, a magnetic resonance imaging (MRI) evaluation of the pituitary can be done to confirm the diagnosis. An empty sella is present in about 70% of patients, and a partially empty sella is present in about 30% of patients on a later MRI.[10] Acute Sheehan syndrome signs on an MRI may demonstrate acute central infarction without hemorrhage in an enlarged pituitary. As the disease progresses, the MRI may show pituitary gland atrophy and eventually a partial or empty sella.[11]

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