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The adrenal cortex produces steroid hormones called

However, despite continual effort, successful separation of clinical efficacy from deleterious side effects has not been achieved. Consequently, chronic use of these powerful drugs is limited by their slow, cumulative side-effect profile. The damage associated with corticosteroid therapy may not become apparent until the consequences are catastrophic. The adrenal cortex comprises three zones: the zonae glomerulosa, fasciculata, and reticularis.

Aldosterone, the major bioactive mineralocorticoid in humans, is synthesized in the outermost zona glomerulosa. This region of the adrenal cortex is regulated by circulating sodium, potassium, and angiotensin. The inner zonae fasciculata and reticularis produce both cortisol and corticosterone. These regions of the adrenal, and to a much lesser extent the zona glomerulosa, are regulated by ACTH released from the anterior pituitary. Five classes of steroid hormones are produced in the adrenal cortex: glucocorticoids, mineralocorticoids, progestins, androgens, and estrogens.

However, the amount of progestin, androgen, and estrogen produced by the adrenal is a minor fraction of the total amount of these steroids produced in the body. By contrast, glucocorticoids and mineralocorticoids are produced almost exclusively in the adrenal cortex.

Glucocorticoids have a broad physiologic role that includes both regulation of glucose metabolic pathways and modulation of the immune system. Mineralocorticoids are key regulators of mineral and water balance. Corticosteroid biosynthesis has been well characterized, and is presented in simplified form in Figure Cholesterol, the precursor to all steroid biosynthetic pathways, is converted to a variety of steroid molecules in a series of reactions catalyzed by several cytochrome P cyp enzymes.

After synthesis, corticosteroids are rapidly secreted. Because corticosteroids are not stored in the adrenal cortex, the rate of steroid synthesis is essentially equal to the rate of secretion from the adrenal gland. Principal pathways for the biosynthesis of adrenocorticosteroids. Reproduced with permission from Haynes and Murad. By agreement with the publisher, this book is accessible by the search feature, but cannot be browsed. Turn recording back on.

National Center for Biotechnology Information , U. Search term. The steroids that are made almost exclusively in the adrenal glands are cortisol, deoxycortisol, aldosterone, corticosterone, and deoxycorti-costerone. Most other steroid hormones, including the estrogens, are made by the adrenal glands and the gonads [ 1 ].

The mineralocorticoids are formed in the zona glomerulosa. The main function of the mineralocorticoids is to promote tubular reabsorption of sodium and secretion of potassium and hydrogen ions at the collecting tubule, distal tubule, and collecting ducts [ 2 ].

When sodium is reabsorbed, water is absorbed simultaneously. The absorption of sodium and water increases fluid volume and arterial pressure. Mineralocorticoid potency in descending order is: aldosterone, deoxycorticosterone, oxocortisol, corticosterone, and cortisol [ 1 ]. Although cortisol has mainly glucocorticoid activity, it also has some mineralocorticoid activity.

Corticosterone has mainly glucocorticoid activity and some mineralocorticoid activity. Aldosterone secretion is regulated primarily by the renin-angiotensin system; it also is stimulated by increased serum potassium concentrations. Hyperkalemia and angiotensin II cause an increase in aldosterone. To a lesser degree, elevated sodium concentration suppresses aldosterone secretion and corticotropin allows aldosterone secretion.

The glucocorticoids are produced primarily in the zona fasciculata. The glucocorticoids affect metabolism in several ways. Glucocorticoids stimulate gluconeogenesis and decrease the glucose use by cells. Cortisol reduces protein stores in all cells of the body, except the liver, and increases protein synthesis in the liver. Cortisol also increases amino acids in the blood, decreases transport of amino acids into extrahepatic cells, and increases transport of amino acids into hepatic cells.

Cortisol mobilizes fatty acids from adipose tissue, increases free fatty acids in the plasma, and increases free fatty acid use for energy. Corticosterone accounts for a small, but significant, amount of the total glucocorticoid activity. Cortisol secretion is regulated almost entirely by corticotropin, which is secreted by the anterior pituitary gland in response to corticotropin-releasing hormone CRH from the hypothalamus.

Serum cortisol inhibits secretion of CRH and corticotropin, which prevents excessive secretion of cortisol from the adrenal glands. Corticotropin stimulates cortisol secretion and promotes growth of the adrenal cortex in conjunction with growth factors, such as insulin-like growth factor IGF -1 and IGF There is a circadian rhythm to cortisol secretion; the highest cortisol levels occur about 1 hour before arising. Stress, pain, and inflammation cause increased cortisol production.

In men, androgens are responsible for the development of secondary sexual characteristics. The androgens play a less important role in women; however, the adrenal androgens are responsible for much of the growth of pubic and axillary hair. Testosterone is the major androgen. Androgens are produced in the adrenal glands and the gonads. The adrenal androgens are formed primarily in the zona reticularis. Dehydroepiandrosterone DHEA is the principal steroid that is produced by the adrenal glands.

Adrenal androgens are moderately active male sex hormones. Some of the adrenal androgens are converted to testosterone. The mechanism of stimulation of androgen secretion from the adrenals is not well understood. Adrenarche is the maturation of the adrenals, which causes an increase in these androgens and occurs between age 5 and 20 [ 5 ].

Adrenarche, therefore, begins well before puberty. Adrenal androgen secretion is regulated partially by corticotropin but also by other unknown factors. The testes secrete testosterone, dihydrotestosterone DHT , and androstenedione. Gonadal production of androgens is controlled by hypothalamic secretion of GnRH, which causes the anterior pituitary to release follicle-stimulating hormone FSH and luteinizing hormone LH.

Testosterone is secreted by the Leydig cells of the testes in response to LH stimulation. Most of the testosterone is converted to the more active DHT in the target tissues. In women, the main function of estrogens is to promote proliferation and growth of specific cells in the body that are responsible for the development of most of the secondary sexual characteristics.

The progestins are responsible for the preparation of the uterus for pregnancy and the breasts for lactation. In men, estrogens and progestins usually do not play a clinically significant role in the development of sexual characteristics. In women, estrogens and progestins are derived from the adrenal gland or the gonad. In women who have intact ovaries, the adrenal contribution to circulating estrogens is insignificant. Estrogens and progestins are secreted in differing rates during the different parts of the female menstrual cycle.

Estradiol is the prominent ovarian estrogen; estrone and estriol are two other estrogens. Estradiol is 12 times as potent as estrone and 80 times as potent as estriol [ 3 ]. Estrone is made in small amounts by the ovaries, but mostly is formed by peripheral conversion from androgens. Estriol is mainly a metabolite of estrone and estradiol in nonpregnant women. In pregnancy, however, estriol is the major estrogen of the placenta. DHEA-S from the fetal adrenal glands is converted to estriol by the placenta.

The major progestin is progesterone; a minor progestin is hydroxy-progesterone. In the first half of the menstrual cycle, small amounts of progesterone are produced—about half from the ovaries and about half from the adrenal cortex. Larger amounts of progesterone are secreted in the latter half of the menstrual cycle by the corpus luteum. The Sertoli cells convert a small amount of testosterone to estrogen.

Also, estrogens are formed from testosterone and androstenediol peripherally in the liver. Cortisol combines with cortisol-binding globulin CBG and albumin. Only the free portion of cortisol is active. Some clinical situations can cause an increase or decrease in the CBG. For example, an increase in estrogens or in thyroid hormone can cause an increase in the CBG.

Alternately, hypothyroidism, increased androgens, acute stress, and nephrotic syndrome can cause a decreased CBG. A change in the amount of CBG affects the total cortisol level, but not the free cortisol level. Also, cortisone, corticosterone, deoxycorticosterone, progesterone, and hydroxyprogesterone bind to CBG [ 1 ].

Testosterone and estradiol are bound to sex hormone—binding globulin SHBG , which is sometimes referred to as testosterone binding globulin. Androstenedione and DHEA are bound weakly to albumin. Estrogen, diabetes mellitus, hyperthyroidism, and cirrhosis can cause an increase in SHBG, whereas testosterone and age can cause a decrease in SHBG [ 8 ]. Cortisol and aldosterone either become fixed in the target tissue or degraded in the liver.

The half-life of cortisol is 60 to minutes. The half-lives of aldosterone, DHEA, androstenedione, testosterone, and estradiol are less than 20 minutes. The half-life of aldosterone is less than 15 minutes. Unmetabolized cortisol accounts for about 0.

Other causes are idiopathic hyperaldosteronism, primary adrenal hyperplasia, dexamethasone suppressible hyperaldosteronism, and adrenal cortical carcinoma. Primary hyperaldosteronism is distinguished from other causes of hyperaldosteronism by a high plasma aldosterone PA level and a low plasma renin activity PRA. Secondary hyperaldosteronism with hypertension can be caused by renal artery stenosis, a renin-secreting tumor, malignant hypertension, or chronic renal disease.

Secondary hyperaldosteronism with nor-motension can be caused by renal disorders eg, renal tubular acidosis or Barters syndrome , diuretic or laxative use, cirrhosis, congestive heart failure, vomiting, and familial chloride diarrhea. Measurement of aldosterone concentration by itself is not a useful screening test because there is overlap between primary hyperaldosteronism, secondary hyperaldosteronism, and essential hypertension. After a diagnosis of primary hyperaldosteronism is suspected based on the ratio of PA:PRA, the usual next step is confirmatory testing to demonstrate the autonomy of aldosterone secretion.

This can be performed by giving two liters of saline over 4 hours and looking for possible aldosterone suppression. Lack of cortisol can be caused by an inability of the adrenal glands to produce cortisol primary adrenal insufficiency or by lack of CRH or corticotropin secondary or tertiary adrenal insufficiency. In secondary and tertiary adrenal insufficiency, the adrenal glands are able to make aldosterone because of intact stimulation of the adrenal glands by angiotensin II but not cortisol.

Primary adrenal insufficiency has several causes, including autoimmune disease; adrenal hemorrhage; HIV; or infiltration of the adrenals by tuberculosis, sarcoidosis, or amyloidosis. Causes of secondary or tertiary adrenal insufficiency are infiltration of the anterior pituitary or hypothalamus by craniopharyngioma, pituitary adenoma, metastasis, sarcoidosis, or tuberculosis or by suppression of corticotropin by long-term steroid use. Chronically, adrenal insufficiency can manifest with weakness, fatigue, anorexia, nausea, abdominal pain, and diarrhea.

Hyponatremia can be present in any form of adrenal insufficiency. Hyperkalemia can be present in primary adrenal insufficiency because of the lack of aldosterone. In acute adrenal insufficiency, patients may be hypotensive from decreased vascular tone, decreased cardiac output, and relative hypovolemia. If untreated, adrenal insufficiency can lead to coma and death. Evaluation of adrenal insufficiency usually is performed by measurement of serum cortisol.

Because of the diurnal pattern of cortisol secretion, random cortisol levels are of little value. In the outpatient setting, the preferred tests are either a morning cortisol or a corticotropin-stimulation test. If acute secondary adrenal insufficiency is suspected, another type of stimulation test, such as a CRH-stimulation test, must be used to rule out adrenal insufficiency. Complicating factors in the evaluation of serum cortisol levels during acute stress are that the albumin and CBG may decrease.

Therefore, the total serum cortisol may be decreased even if the level of free active cortisol is unchanged [ 11 ] Methods have been developed for measuring serum free cortisol; however, they are technically demanding, expensive, and are not readily available [ 12 ].

A ratio of cortisol:CBG has been proposed to determine a free cortisol index that is proportionate to the serum free cortisol [ 13 ]. Corticotropin can be produced by the anterior pituitary gland or by an ectopic source, such as bronchial carcinoid or small cell lung cancer.

Likewise, ectopic production of CRH can be produced by bronchial carcinoid, medullary thyroid cancer, or metastatic prostate cancer. Clinical manifestations of excess cortisol include hypertension, diabetes mellitus, androgen-type hirsutism, irregular menses, weight gain, ecchymoses, myopathy, osteopenia, truncal obesity, and purple striae. Alternately, a 1-mg overnight dexamethasone suppression test often is used for screening purposes. In this test, 1 mg of dexamethasone is taken orally at 10 pm or 11 pm and a cortisol level is obtained at 8 am the next morning [ 14 ].

Because the serum free cortisol diffuses freely into saliva, the salivary cortisol reflects the serum free cortisol level [ 15 ]. Saliva can be collected at various times of the day as an outpatient, which allows serial cortisol measurements without performing serial blood draws [ 16 ]. Tests of gonadal function are most commonly performed in men for hypogonadism and in women for menstrual disorders, hirsutism, and virilization. Usually, LH and FSH are measured along with the androgens or estrogens to help determine the cause of the problem.

There are many causes of male sexual dysfunction. One of the causes is a disorder of the hypothalamic-pituitary-gonadal axis. A good screening test is measurement of serum total testosterone level in the morning. FSH and LH can be measured simultaneously to help determine the cause of the disorder. Most symptoms are secondary to polycystic ovarian syndrome or idiopathic hirsutism. The best test to rule out an androgen-secreting tumor is a serum total testosterone and a serum DHEA-S.

Congenital adrenal hyperplasia CAH is another clinical disease that affects the levels of steroid hormones that are produced by the adrenal cortex. Congenital adrenal hyperplasia is a group of inherited diseases that result in defective activity of one of five enzymes in the adrenal cortex.

The defective enzyme leads to decreased production of cortisol, and, therefore, an increased production of corticotropin, excess production of hormones proximal to the enzyme defect, and glandular enlargement. In the classic form of salt-wasting hydroxylase deficiency CAH, girls are born with ambiguous genitalia and boys and girls may have Addisonian crisis and hypotension. In simple virilizing hydroxylase CAH, girls express ambiguous genitalia but do not experience Addisonian crisis.

Boys who have hydroxylase CAH are not ambiguous. Untreated male nonsalt losers present with precocious puberty. Like girls who have salt-losing hydroxylase CAH, boys present with Addisonian crisis in the first few weeks of life. The frequency of CAH is about 1 in 14, [ 19 ]. The nonclassic form of 21 hydroxylase deficiency is more common 1 in and presents at puberty in girls who have signs of excess androgen [ 20 ].

A deficiency in hydroxylase causes an increase in the hormone hydroxyprogesterone, as well as excess testosterone and DHEA-S. Immunoassays IAs are among the most sensitive and precise analytical methods; however, recent studies [ 23 — 36 ] showed that many immunoassays lack specificity as a result of cross-reactivity. Furthermore, results from the College of American Pathologists Proficiency Testing Program for the year Y-survey [ 36 ] clearly showed that the antibodies that are used in the commercially available immunoassays for steroids lack specificity.

In the past, steroids usually were analyzed individually, using gas chromatography-mass spectrometry GC-MS or immunoassay. GC-MS is sensitive and specific, but requires tedious and time-consuming sample preparation, whereas it is clear that immunoassays lack specificity.

Liquid chromatography-mass spectrometry LC-MS and liquid chromatography-tandem mass spectrometry are specific and offer simpler approaches to sample preparation without sample derivatization steps. Recently, several LC-MS—based methods that use different ion sources were reported for the determination of the following steroid hormones: testosterone [ 37 — 39 ], cortisol [ 40 — 44 ], deoxycortisol [ 45 ], androstenedione [ 38 , 39 ], DHEA [ 46 ], DHEA-S [ 38 , 46 ], progesterone [ 47 ], hydroxyprogesterone [ 48 ], estriol [ 49 ], and estradiol [ 38 , 49 ].

Without multi-step sample preparation procedures, the APCI source usually cannot provide adequate sensitivity for some steroids, such as estradiol and DHEA, in human serum. For the nonpolar or low polar compounds, such as most steroid molecules, the sensitivity that is provided by the ESI source is less satisfactory [ 44 , 48 ] than the APCI source.

Alary [ 51 ] used APPI-tandem mass spectrometry for the detection of steroids in biologic matrices. In selected ion monitoring mode and multiple reaction monitoring MRM mode, the signal that was obtained by photoionization was more intense by a factor of 3 to 10 when compared with the APCI source.

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This chapter reviews the pharmacology and physiology of corticosteroids, discusses the use of these hormonal agents in the treatment of neoplasms and presents the mechanism of action currently known for corticosteroids in the context of their therapeutic efficacy.

Already in the mid-nineteenth century, it was observed that the lack of functional adrenal glands is incompatible with life. Subsequent research classified the effects of adrenal insufficiency into two distinct groups: those due to electrolyte imbalance and those due to alterations.

The hypercortical syndrome was described by Cushing in and in the s and s, the adrenocorticotropic hormone ACTH was identified in the anterior part of the pituitary gland and was described as a stimulator of the adrenal cortex.

During this time, several bioactive steroids, including cortisol and aldosterone the main active corticosteroids in humans were isolated from the adrenal cortex and characterized. In , Hench reported for the first time on the efficacy of cortisol and ACTH in the treatment of rheumatoid arthritis , an observation that quickly extended to therapeutic applications in a wide variety of diseases.

The intense investigation of these compounds was stimulated by this broad clinical interest, and in the following decade, most of the biochemistry involved in the synthesis and metabolism of adrenocortical steroids was elucidated. During this period, the field of corticosteroid therapy progressed rapidly since most of the currently available synthetic corticosteroid analogues were developed and practical methods of determining cortisol in plasma were identified.

In the intervening years, analogs of synthetic corticosteroids were developed that separate the effects of anti-inflammatory and electrolyte balance. However, despite the continuous effort, the successful separation of clinical efficacy from harmful side effects has not been achieved. Consequently, the chronic use of these powerful drugs is limited by their slow and cumulative profile of side effects.

The damage associated with corticosteroid therapy may not be apparent until the consequences are catastrophic. Five classes of steroid hormones are produced in the adrenal cortex: glucocorticoids, mineralocorticoids, progestins, androgens, and estrogens. However, the amount of progestin, androgen, and estrogen produced by the adrenal gland is a smaller fraction of the total amount of these steroids produced in the body. In contrast, glucocorticoids and mineralocorticoids occur almost exclusively in the adrenal cortex.

Glucocorticoids have a broad physiological role that includes both the regulation of the metabolic pathways of glucose and the modulation of the immune system. Mineralocorticoids are key regulators of the water and mineral balance. Corticosteroid biosynthesis has been well characterized. As noted earlier, the adrenal cortex releases glucocorticoids in response to long-term stress such as severe illness.

In contrast, the adrenal medulla releases its hormones in response to acute, short-term stress mediated by the sympathetic nervous system SNS. The medullary tissue is composed of unique postganglionic SNS neurons called chromaffin cells that produce the neurotransmitters epinephrine also called adrenaline and norepinephrine also called noradrenaline , which are chemically classified as catecholamines. Epinephrine is produced in greater quantities and is the more powerful hormone. The secretion of medullary epinephrine and norepinephrine is controlled by a neural pathway that originates from the hypothalamus in response to danger or stress.

Both epinephrine and norepinephrine increase the heart rate, pulse, and blood pressure to prepare the body to fight the perceived threat or flee from it. In addition, the pathway dilates the airways, raising blood oxygen levels. It also prompts vasodilation, further increasing the oxygenation of important organs such as the lungs, brain, heart, and skeletal muscle while also prompting vasoconstriction to blood vessels serving less essential organs such as the gastrointestinal tract, kidneys, and skin.

It also downregulates some components of the immune system. Other effects include a dry mouth, loss of appetite, pupil dilation, and a loss of peripheral vision. Several disorders are caused by the dysregulation of the hormones produced by the adrenal glands. It is caused by hypersecretion of cortisol.

Addisonian crisis is a life-threatening condition due to severely low blood pressure resulting from a lack of corticosteroid levels. Before initiating long-term systemic corticosteroid therapy, a thorough history and physical examination should be performed to assess for risk factors or pre-existing conditions that may potentially be exacerbated by glucocorticoid therapy, such as diabetes, dyslipidemia, cerebrovascular disease CVD , GI disorders, affective disorders, or osteoporosis.

At a minimum, baseline measures of body weight, height, bone mineral density, and blood pressure should be obtained, along with laboratory assessments that include a complete blood count CBC , blood glucose values, and lipid profile. In children, nutritional and pubertal status should also be examined. Concomitant use of other medications should also be assessed before initiating therapy as significant drug interactions have been noted between glucocorticoids and several drug classes.

Females of childbearing age should also be questioned about the possibility of pregnancy because use in pregnancy may increase the risk of cleft palate in offspring. Long-term corticosteroid therapy should never be stopped abruptly due to its effect on the hypothalamic-pituitary-adrenal HPA axis and potential adrenal suppression.

Instead, the dose should be tapered to allow the body to resume natural production of adrenal hormone levels. Patients on long-term corticosteroid therapy who are also at high risk for fractures are recommended to receive concurrent pharmacological treatment for osteoporosis. The lowest effective dose should be used for treatment of the underlying condition, and the dose should be re-evaluated regularly to determine if further reductions can be instituted.

Health care professionals should monitor for adrenal suppression in patients who have been treated with corticosteroids for greater than two weeks or in multiple short courses of high-dose therapy. If these symptoms occur, further lab work, such as an early morning cortisol test, should be performed.

Corticosteroids are used as replacement therapy in adrenal insufficiency, as well as for the management of various dermatologic, ophthalmologic, rheumatologic, pulmonary, hematologic, and gastrointestinal GI disorders. In respiratory conditions, systemic corticosteroids are used for the treatment of acute exacerbations of chronic obstructive pulmonary disease COPD and severe asthma.

Mineralocorticoids are primarily involved in the regulation of electrolyte and water balance. Glucocorticoids are predominantly involved in carbohydrate, fat, and protein metabolism and also have anti-inflammatory, immunosuppressive, anti-proliferative, and vasoconstrictive effects. Prednisone is perhaps the most widely used of the systemic corticosteroids.

It is generally used as an anti-inflammatory and immunosuppressive agent. Figure 9. Despite their beneficial effects, long-term systemic use of corticosteroids is associated with well-known adverse events, including osteoporosis and fractures, adrenal suppression, hyperglycemia and diabetes, cardiovascular disease and dyslipidemia, dermatological and GI events, psychiatric disturbances, and immunosuppression.

One side effect that is unique to children is growth suppression. When reduction in dosage is possible, the reduction should be gradual and should not be stopped abruptly because of the associated HPA suppression that occurs with long-term administration. This hypothalamus-pituitary-adrenal HPA suppression can cause an impaired stress response, which may persist for months after discontinuation of therapy; therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted.

Alternate day therapy is a corticosteroid dosing regimen in which twice the usual daily dose of corticoid is administered every other morning. The purpose of this mode of therapy is to minimize undesirable effects that can occur during long-term administration. Dosages are variable and tailored to the disease process and the individual.

Corticosteroids may mask some signs of infection, and new infections may appear during their use. Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes to severe depression. Glucocorticoid medication can cause immunosuppression, which makes it more difficult to detect signs of infection.

Patients should seek advice from healthcare providers regarding vaccination administration while on glucocorticoids. Patients should report unusual swelling, weight gain, fatigue, bone pain, bruising, non-healing sores, visual and behavioral disturbances to the provider. Use of glucocorticoid therapy may cause an increase in blood glucose levels. Patients should be advised to consume diets that are high in protein, calcium, and potassium.

Medication grids are intended to assist students to learn key points about each medication. Because information about medication is constantly changing, nurses should always consult evidence-based resources to review current recommendations before administering specific medication.

Basic information related to each class of medication is outlined below. Detailed information on a specific medication can be found for free at Daily Med at dailymed. On the home page, enter the drug name in the search bar to read more about the medication.

May require concurrent treatment for osteoporosis or elevated blood glucose levels. Apply a small amount of medication to cover the affected area of skin with a thin, even film and rub in gently. Symptoms should begin to improve during the first few days of treatment; do not use this medication longer than 7 days unless directed. Continually monitor for signs that indicate dosage adjustment is necessary, such as exacerbations of the disease or stress surgery, infection, trauma.

Critical Thinking Activity 9. A patient in a long-term care facility who has COPD receives prednisone 10 mg daily to help manage her respiratory status. The nurse is concerned because the patient requires assistance and is a fall risk so the nurse plans to call the provider.

Mineralocorticoids: Aldosterone The most superficial region of the adrenal cortex is the zona glomerulosa, which produces a group of hormones collectively referred to as mineralocorticoids because of their effect on body minerals, especially sodium and potassium. Glucocorticoids: Cortisol The intermediate region of the adrenal cortex produces hormones called glucocorticoids because of their role in glucose metabolism.

Androgens The deepest region of the adrenal cortex produces small amounts of a class of steroid sex hormones called androgens.


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Each adrenal gland weighs 4—5 g in an adult. Adrenals are first detected at 6 weeks' gestation. Each adrenal gland is composed of two distinct parts: the outer part called the adrenal cortex and the inner adrenal medulla.

The adrenal glands secrete different hormones which act as 'chemical messengers'. These hormones travel in the bloodstream and act on various body tissues to enable them to function correctly. All adrenocortical hormones are steroid compounds made from cholesterol. Adrenocorticotropic hormone ACTH , secreted by the anterior pituitary gland , primarily affects release of glucocorticoids and adrenal androgens by the adrenal gland and, to a much lesser extent, also stimulates aldosterone release.

Catecholamines include adrenaline , noradrenaline and small amounts of dopamine — these hormones are responsible for all the physiological characteristics of the stress response, the so called 'fight or flight' response. This causes high blood pressure, which is resistant to conventional blood pressure control tablets, and salt disturbances.

High blood pressure may cause headaches and visual problems. In rare cases, the adrenal glands can become either overactive or underactive. The two main glucocorticoid-related disorders resulting from these are Cushing's syndrome and Addison's disease , respectively. Cushing's syndrome is due to overactive adrenal glands from excessive production of cortisol.

The clinical findings include thinning and bruising of the skin, obesity , diabetes , psychiatric disturbances, high blood pressure, muscle weakness, osteoporosis , excessive facial hair and irregular periods in women. It can result in growth failure in children.

Patients with cortisol excess also have impaired wound healing and an increased susceptibility to infection. Addison's disease or adrenal insufficiency is due to underactive adrenal glands associated with lack of hormones. Adrenal insufficiency may be acute or chronic. Symptoms of chronic adrenal insufficiency include low blood pressure, fatigue, weight loss, anorexia, nausea, vomiting, abdominal pain, salt craving and low blood sugar.

Skin and mucous membranes may show increased pigmentation. The loss of secondary sex characteristics is seen only in women with the disease. Acute adrenal insufficiency is a medical emergency and must be identified and promptly treated. The hallmarks of acute adrenal insufficiency are circulatory collapse with abdominal pain and low blood sugar. Overproduction of androgens is also very rare but may result in excessive hair growth and menstrual period disturbances. Tumours of the adrenal gland are mostly benign and do not result in over or underproduction of adrenal hormones.

Most tumours are discovered incidentally when people undergo scans for various other reasons. Adrenal cancer is very rare. Adrenal tumours may require surgery if they are large or overproduce hormones. The treatment of each disorder varies according to the specific cause. Patients with any concerns about these conditions should seek advice from their doctor. Hormone replacement therapy or HRT also known as menopausal hormone therapy; MHT is the replacement of female sex hormones oestrogen and progesterone in women to control symptoms of the menopause.

It produces steroid hormones such as cortisol, aldosterone, and hormones that can be changed into testosterone. The inner part of the gland is called the medulla. It produces epinephrine and norepinephrine. These hormones are also called adrenaline and noradrenaline. When the glands produce more or less hormones than normal, you can become sick. This might happen at birth or later in life. The adrenal glands can be affected by many diseases, such as autoimmune disorders , infections, tumors , and bleeding.

Some are permanent and some go away over time. Medicines can also affect the adrenal glands. The pituitary, a small gland at the bottom of the brain, releases a hormone called ACTH that is important in stimulating the adrenal cortex. Pituitary diseases can lead to problems with adrenal function. Friedman TC. Adrenal gland. Andreoli and Carpenter's Cecil Essentials of Medicine. Philadelphia, PA: Elsevier Saunders; chap The adrenal cortex.