{"id":381,"date":"2019-11-15T19:10:34","date_gmt":"2019-11-15T19:10:34","guid":{"rendered":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/chapter\/9-3-corticosteriods\/"},"modified":"2025-01-16T22:29:16","modified_gmt":"2025-01-16T22:29:16","slug":"9-3-corticosteriods","status":"publish","type":"chapter","link":"https:\/\/pressbooks.ccconline.org\/accnursingpharmacology\/chapter\/9-3-corticosteriods\/","title":{"raw":"9.3 Corticosteriods","rendered":"9.3 Corticosteriods"},"content":{"raw":"
\n\nThis section will review the anatomy and physiology of the adrenal gland, outline common disorders affecting the adrenal gland, apply the nursing process to administering corticosteroids, and then discuss the medication classes of corticosteroids.\n

Review Anatomy and Physiology of the Adrenal Glands<\/h2>\nThe adrenal gland consists of the adrenal cortex that is composed of glandular tissue and the adrenal medulla that is composed of nervous tissue. Each region secretes its own set of hormones.\n\nThe adrenal cortex is a component of the [pb_glossary id=\"587\"]hypothalamic-pituitary-adrenal (HPA) axis[\/pb_glossary]<\/strong>. The hypothalamus stimulates the release of ACTH from the pituitary, which then stimulates the adrenal cortex to produce steroid hormones that are important for the regulation of the stress response, blood pressure and blood volume, nutrient uptake and storage, fluid and electrolyte balance, and inflammation.\n\nThe [pb_glossary id=\"588\"]adrenal medulla[\/pb_glossary]<\/strong> is neuroendocrine tissue composed of postganglionic sympathetic nervous system (SNS) neurons that secrete the hormones epinephrine and norepinephrine. It is an extension of the autonomic nervous system, which regulates homeostasis in the body. See Figure 9.5[footnote]\u201c<\/span>1818 The Adrenal Glands.jpg<\/a>\u201d by\u00a0<\/span>OpenStax<\/a>\u00a0is licensed under<\/span>\u00a0CC BY 4.0<\/a>. Access for free at\u00a0<\/span>https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/17-6-the-adrenal-glands<\/a>[\/footnote]<\/span>\u00a0for an illustration of the adrenal gland and associated hormones.\n\n[caption id=\"\" align=\"aligncenter\" width=\"1102\"]\"Illustration Figure 9.5 Adrenal Gland and Associated Hormones[\/caption]\n\nOne of the major functions of the adrenal gland is to respond to stress. The body responds in different ways to short-term stress and long-term stress following a pattern known as the [pb_glossary id=\"589\"]general adaptation syndrome (GAS)[\/pb_glossary]<\/strong>. Stage one of GAS is called the alarm reaction. This is short-term stress, also called the fight-or-flight response, and is mediated by the hormones epinephrine and norepinephrine from the adrenal medulla. Their function is to prepare the body for extreme physical exertion. If the stress is not soon relieved, the body adapts to the stress in the second stage called the stage of resistance. If a person is starving for example, the body may send signals to the gastrointestinal tract to maximize the absorption of nutrients from food. If the stress continues for a longer term however, the body responds with symptoms such as depression, suppressed immune response, or severe fatigue. These symptoms are mediated by the hormones of the adrenal cortex, especially cortisol.\n\nAdrenal hormones also have several nonstress-related functions, including the increase of blood sodium and glucose levels, which will be described in further detail below.\n

Mineralocorticoids: Aldosterone<\/h3>\nThe most superficial region of the adrenal cortex is the zona glomerulosa, which produces a group of hormones collectively referred to as [pb_glossary id=\"590\"] mineralocorticoids[\/pb_glossary]<\/strong> because of their effect on body minerals, especially sodium and potassium. These hormones are essential for fluid and electrolyte balance. [pb_glossary id=\"591\"]Aldosterone[\/pb_glossary]<\/strong> is the major mineralocorticoid that is important in the regulation of the concentration of sodium and potassium ions in the body. The secretion of aldosterone by the adrenal cortex is prompted by the HPA axis when the hypothalamus triggers ACTH release from the anterior pituitary. It is released in response to elevated blood levels of potassium (K+), low blood levels of sodium (Na+), low blood pressure, or low blood volume. Aldosterone targets the kidneys and increases the excretion of K+ and the retention of Na+, which, in turn, causes the retention of water, thus increasing blood volume and blood pressure.\n\nAldosterone is also a key component of the renin-angiotensin-aldosterone system (RAAS) in which specialized cells of the kidneys secrete renin in response to low blood volume or low blood pressure. Renin then catalyzes the conversion of the blood protein angiotensinogen, which is produced by the liver, to the hormone Angiotensin I. Angiotensin I is converted in the lungs to Angiotensin II by the angiotensin-converting enzyme (ACE). Angiotensin II has three major functions: initiating vasoconstriction of the arterioles, thus decreasing blood flow; stimulating kidney tubules to reabsorb sodium and water, thus increasing blood volume; and signaling the adrenal cortex to secrete aldosterone, which further increases blood volume and blood pressure. It is important to understand these effects because many cardiac medications target the effects of aldosterone and the RAAS system. For example, drugs that block the production of Angiotensin II are known as ACE inhibitors. ACE inhibitors are used to help lower blood pressure in clients with hypertension by blocking the ACE enzyme from converting Angiotensin I to Angiotensin II, which, in turn, causes vasodilation of the arterioles. Another medication called spironolactone is used as a diuretic because it blocks the effects of aldosterone and, thus, causes the kidneys to eliminate water and sodium to decrease blood volume and blood pressure.\n

Glucocorticoids: Cortisol<\/h3>\nThe intermediate region of the adrenal cortex produces hormones called glucocorticoids because of their role in glucose metabolism. In response to long-term stressors, the HPA axis triggers the release of glucocorticoids. Their overall effect is to inhibit tissue building while stimulating the breakdown of stored nutrients to maintain adequate fuel supplies. In conditions of long-term stress, cortisol promotes the catabolism of glycogen to glucose, stored triglycerides into fatty acids and glycerol, and muscle proteins into amino acids. These raw materials can then be used to synthesize additional glucose and ketones for use as body fuels. However, the negative effects of catabolism for energy can result in muscle breakdown and weakness, poor wound healing, and the suppression of the immune system.\n\nMany medications contain glucocorticoids to treat various conditions, such as cortisone injections for inflamed joints; prednisone tablets, IV medications, and steroid-based inhalers to manage inflammation that occurs in asthma; and hydrocortisone creams that are applied to relieve itchy skin rashes.\n

Androgens<\/h3>\nThe deepest region of the adrenal cortex produces small amounts of a class of steroid sex hormones called androgens. During puberty and most of adulthood, androgens are produced in the gonads. The androgens produced in the adrenal cortex supplement the gonadal androgens.\n

Adrenal Medulla: Epinephrine and Norepinephrine<\/h3>\nAs 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.\n\nThe 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.\n

Disorders Involving the Adrenal Glands<\/h2>\nSeveral disorders are caused by the dysregulation of the hormones produced by the adrenal glands. For example, Cushing\u2019s disease is a disorder characterized by high blood glucose levels, the development of a moon-shaped face, a buffalo hump on the back of the neck, rapid weight gain, and hair loss. It is caused by hypersecretion of cortisol as the result of an ACTH-producing pituitary tumor. Cushing\u2019s syndrome can also be caused by long-term use of corticosteroid medications.\n\nIn contrast, the hyposecretion of corticosteroids can result in Addison\u2019s disease, a disorder that causes low blood glucose levels and low blood sodium levels. Addisonian crisis is a life-threatening condition due to severely low blood pressure resulting from a lack of corticosteroid levels.[footnote]This work is a derivative of Anatomy and Physiology<\/a> by OpenStax<\/a> licensed under CC BY 4.0<\/a>. Access for free at https:\/\/openstax.org\/books\/anatomy-and-physiology\/pages\/1-introduction<\/a>[\/footnote],[footnote]This work is a derivative of DailyMed<\/a> by U.S. National Library of Medicine<\/a> in the Public Domain<\/a>.[\/footnote],[footnote]Nieman, L., Biller, B., Findling, J., Murad, M., Newell-Price, J., Savage, M., & Tabarin, A. (2015, August 1). Treatment of Cushing\u2019s syndrome: An endocrine clinical practice guideline. The Journal of Clinical Endocrinology & Metabolism, 100<\/em>(8), 2807-2831. https:\/\/academic.oup.com\/jcem\/article\/100\/8\/2807\/2836065<\/a>[\/footnote],[footnote]Liu, D., Ahmet, A., Ward, L., et al. (2013). A practical guide to the monitoring and management of the complications of systemic corticosteroid therapy. Allergy, Asthma & Clinical Immunology, 9<\/em>, 30. https:\/\/aacijournal.biomedcentral.com\/articles\/10.1186\/1710-1492-9-30<\/a>[\/footnote]<\/sup>\n\nView a\u00a0 supplementary YouTube video about ACTH and the adrenal gland:\n
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ACTH and the Adrenal Gland[footnote]Forciea, B. (2015, May 12). Anatomy and physiology: Endocrine system: ACTH<\/em> (Adrenocorticotropin Hormone) V2.0 [Video]. YouTube. All rights reserved. Video used with permission. https:\/\/youtu.be\/4m7XflJzm2w<\/a>. [\/footnote]<\/sup><\/h3>\n[embed]https:\/\/www.youtube.com\/watch?v=4m7XflJzm2w[\/embed]\n\n<\/div>\n

Applying the Nursing Process to Corticosteroids<\/h2>\n

Assessment<\/h3>\nBefore initiating long-term systemic corticosteroid therapy, a thorough history and physical examination should be performed to assess for risk factors or preexisting 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. Symptoms of and\/or exposure to serious infections should also be assessed as corticosteroids are contraindicated in clients with untreated systemic infections. 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.[footnote]Liu, D., Ahmet, A., Ward, L., Krishnamoorthy, P., Mandelcorn, E., Leigh, R., Brown, J., Cohen, A., & Kim, H. (2013, August 15). A practical guide to the monitoring and management of the complications of systemic corticosteroid therapy. Allergy, Asthma & Clinical Immunology, 9<\/em>(30). https:\/\/doi.org\/10.1186\/1710-1492-9-30<\/a>[\/footnote]<\/sup>\n

Implementation<\/h3>\nLong-term corticosteroid therapy should never be stopped abruptly due to the risk of Addisonian crisis. Instead, the dose should be tapered to allow the body to resume natural production of adrenal hormone levels. Addisonian crisis is a potentially life-threatening condition resulting from an acute insufficiency of adrenal hormones that can occur if chronic corticosteroid therapy is suddenly stopped.\n\nClients on long-term corticosteroid therapy who are also at high risk for fractures are recommended to receive concurrent pharmacological treatment for osteoporosis. Alendronate, a bisphosphonates class of medication, is often used, in addition to other osteoporosis preventative measures such as weight-bearing exercise and calcium\/vitamin D supplementation.[footnote]Liu, D., Ahmet, A., Ward, L., Krishnamoorthy, P., Mandelcorn, E., Leigh, R., Brown, J., Cohen, A., & Kim, H. (2013, August 15). A practical guide to the monitoring and management of the complications of systemic corticosteroid therapy. Allergy, Asthma & Clinical Immunology, 9<\/em>(30). https:\/\/doi.org\/10.1186\/1710-1492-9-30<\/a> [\/footnote]<\/sup>\n

Evaluation<\/h3>\nThe lowest effective dose should be used for treatment of the underlying condition, and the dose should be reevaluated regularly to determine if further reductions can be instituted.\n\nThe parameters described under \"Assessment\" should be monitored regularly. Health care professionals should monitor for adrenal suppression in clients who have been treated with corticosteroids for greater than two weeks or in multiple short courses of high-dose therapy. Symptoms of adrenal insufficiency include weakness\/fatigue, malaise, nausea, vomiting, diarrhea, abdominal pain, headache (usually in the morning), poor weight gain and\/or growth in children, myalgia, arthralgia, psychiatric symptoms, hypotension, and hypoglycemia. If these symptoms occur, further lab work, such as an early morning cortisol test, should be performed.[footnote]Liu, D., Ahmet, A., Ward, L., Krishnamoorthy, P., Mandelcorn, E., Leigh, R., Brown, J., Cohen, A., & Kim, H. (2013, August 15). A practical guide to the monitoring and management of the complications of systemic corticosteroid therapy. Allergy, Asthma & Clinical Immunology, 9<\/em>(30). https:\/\/doi.org\/10.1186\/1710-1492-9-30<\/a>[\/footnote]<\/sup>\n

Corticosteroids<\/h2>\nMechanism of Action:<\/strong> Glucocorticoids cause profound and varied metabolic effects as described earlier in this section. In addition, they modify the body's immune responses.[footnote]This work is a derivative of DailyMed<\/a> by U.S. National Library of Medicine<\/a> in the Public Domain<\/a>. [\/footnote]<\/sup>\n\nIndications: <\/strong>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. Hydrocortisone is a commonly used topical cream for itching, and its oral formulation is used to treat Addison\u2019s disease.[footnote]This work is a derivative of DailyMed<\/a> by U.S. National Library of Medicine<\/a> in the Public Domain<\/a>. [\/footnote]<\/sup> Methylprednisolone is a commonly used injectable corticosteroid. Fludrocortisone has much greater mineralocorticoid potency and, therefore, is commonly used to replace aldosterone in Addison's disease.[footnote]Liu, D., Ahmet, A., Ward, L., Krishnamoorthy, P., Mandelcorn, E., Leigh, R., Brown, J., Cohen, A., & Kim, H. (2013, August 15). A practical guide to the monitoring and management of the complications of systemic corticosteroid therapy. Allergy, Asthma & Clinical Immunology, 9<\/em>(30). https:\/\/doi.org\/10.1186\/1710-1492-9-30<\/a> [\/footnote]<\/sup> See Figure 9.6[footnote]\u201c<\/span>Fluticasone.JPG<\/a>\u201d by\u00a0<\/span>James Heilman, MD<\/a>\u00a0is licensed under\u00a0<\/span>CC BY-SA 3.0<\/a>[\/footnote],[footnote]\u201c<\/span>Methylprednisolone vial.jpg<\/a>\u201d by\u00a0<\/span>Intropin<\/a>\u00a0is licensed under\u00a0<\/span>CC BY 3.0<\/a>[\/footnote],[footnote]\u201c<\/span>006035339lg Prednisone 20 MG Oral Tablet.jpg<\/a>\u201d by NLM is licensed under\u00a0<\/span>CC0<\/a>[\/footnote]<\/span>\u00a0for images of various formulations of corticosteroids.\n\n[caption id=\"attachment_380\" align=\"aligncenter\" width=\"1024\"]\"Photos Figure 9.6 Examples of Corticosteroid Medications (fluticasone inhaler, intravenous methylprednisolone, and prednisone tablets)[\/caption]\n\nCorticosteroids are used for a variety of disorders such as the following:\n