Adrenal cortex disorders: Hormones out By Ann Crawford, PhD, RN, MRS. S, 46, IS HOSPITALIZED for Each portion has independent glan- and Helene Harris, MSN, RN treatment of an adrenal gland disor- dular functions. Their hormonal der. On admission, she complained secretions affect organs and tissues of weakness, fatigue, and difficulty throughout the body.1,2 falling and staying asleep. For the The adrenal cortex produces and past 6 weeks, she’s noticed weight secretes hormones known as adrenal 2.3 gain and menstrual irregularities. The steroids or corticosteroids. These are ANCC nurse observes that she has a moon- classified as mineralocorticoids, which CONTACT HOURS face appearance, with an obese trunk help control body fluid and electro- and thin arms and legs. Her skin lyte levels, and glucocorticoids, which appears fragile and parchment-like, are involved in many essential life with scattered ecchymoses and striae processes. The adrenal medulla on her abdomen. She’s slightly tachy- secretes small amounts of catechol- cardic with an elevated BP. Her hus- amines as needed to help with stress band states that Mrs. S has been response requirements.1,2 increasingly irritable and moody Aldosterone, the principal mineral- lately. Is Mrs. S suffering from adre- ocorticoid, maintains extracellular nal cortical insufficiency or adrenal fluid volume as part of the renin- cortical hypersecretion? angiotensin-aldosterone system. This article will describe adrenal Secreted in response to decreased cortical insufficiency (also called extracellular volume, aldosterone Addison disease) and adrenal cortical stimulates the kidneys to reabsorb hypersecretion (also called hypercor- sodium and water and excrete potas- tisolism and Cushing syndrome), and sium in an effort to increase plasma explain how to recognize and man- fluid volume and restore normal age these conditions. For more on osmolality. Other factors that stimu- signs and symptoms, see Recognizing late aldosterone secretion include two adrenal disorders and Lab findings elevated serum potassium levels and for patients with adrenal disorders. adrenocorticotropic hormone (ACTH) stimulation.1 About the adrenal glands Cortisol, the main glucocorticoid, The adrenal glands are highly vascu- influences metabolism of protein, fat, lar, tent-shaped organs located on and carbohydrates, and also affects the top of the kidneys. The outer por- body’s stress response, emotional sta- tion is known as the cortex while bility, and immune function. Cortisol the inner portion is the medulla. release is regulated directly by ACTH 32 l Nursing2012 l October www.Nursing2012.com Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. of kilter (released from the anterior pituitary gland) and indirectly by corticotropin- releasing hormone (CRH), released from the hypothalamus. Low circulating cortisol levels stimulate the hypothalamus to secrete CRH. The increased levels of CRH stimulate ACTH secretion, which in turn stimulates cortisol secretion. Conversely, high cortisol levels in- hibit CRH release, comprising a nega- tive feedback system. The pattern of hormonal secretion is affected by di- urnal cycles as well as physiologic or psychological stress.1–3 Adrenal sex hormones for both genders (primarily androgens) are also secreted by the adrenal cortex, though not in amounts as large as secreted by the gonads. Adrenal cortical insufficiency Primary adrenal cortical insufficiency is a relatively rare disorder also known as Addison disease. It occurs when the adrenal cortex layers are destroyed by autoimmune disorder, tuberculosis, metastatic carcinomas, MAGES I hemorrhage, infections, toxins, or ETTY certain medications (for example, / G ketoconazole or mitotane). Second- COM ary adrenal insufficiency may be RF. caused by hypopituitarism, surgical EDICAL M removal of the pituitary gland, or, BY more commonly, sudden cessation of long-term, high-dose glucocorti- 1,3,4 LLUSTRATION I coid therapy. Tertiary adrenal www.Nursing2012.com October l Nursing2012 l 33 Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. insufficiency is caused by problems glucocorticoid and mineralocorticoid patients with adrenal insufficiency). with the hypothalamus. deficiency, and may develop in a Decreased glucocorticoid secretion Manifestations of adrenal insuffi- slow progression or more quickly impairs the body’s ability to regulate ciency are related primarily to with stress (see Assessment findings in blood glucose levels and to control Recognizing two adrenal disorders1-3 System Addison disease Cushing syndrome Musculoskeletal • Muscle weakness • Muscle weakness and atrophy • Fatigue • Fatigue • Joint or muscle pain • Thin extremities • Osteoporosis • Pathologic fractures • Poor fracture healing Gastrointestinal • Weight loss • Weight gain • Anorexia • Gastric ulcers or bleeding • Nausea and vomiting • Abdominal pain • Constipation or diarrhea Integumentary • Vitiligo • Thinning skin (translucent or parchment-like) • Altered pigmentation (hyperpigmentation and • Striae on the abdomen, thighs, or upper arms “bronzed” appearance with primary Addison • Hyperpigmentation of skin disease, or patchy hypopigmentation) • Ecchymoses • Bluish-black color to gums and oral mucous • Petechiae membranes • Acne • Decreased body, pubic, and axillary • Hirsutism hair (more often in women) • Fine hair on face and body • Male pattern balding (in women) Genitourinary • Menstrual irregularities • Enlarged clitoris Cardiovascular • Orthostatic hypotension • Hypertension • Fluid volume deficit (dehydration) • Tachycardia • Potential for dysrhythmias • Fluid volume overload • Dependent edema • Fragile capillaries Hematologic • Anemia • Increased risk of thrombus formation Neurologic • Headache • Mood swings • Lethargy • Emotional lability • Depression • Irritability • Confusion • Confusion • Mood swings • Difficulty concentrating • Tremors • Depression • Psychotic behaviors • Difficulty sleeping Immune system • Increased risk for infection • Decreased immunity (decreased lymphocytes and immunoglobulin production) • Decreased inflammatory response • Potential masking of infection or inflammation • Decreased neutrophil activity • Decreased production of cytokines, histamines, and prostaglandins Other • Decreased stress tolerance • General appearance: moon face, buffalo hump, • Fever protruding abdomen (truncal obesity) with thin • Salt craving extremities. 34 l Nursing2012 l October www.Nursing2012.com Copyright © 2012 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. the effects of the immune and in- therapy includes hydrocortisone flammatory responses. Reduced cor- for maintenance, with the addition tisol release leads to hypoglycemia of fludrocortisone (a mineralocorti- as glycogen stores are depleted; a coid) for patients who don’t attain decrease in urea nitrogen excretion an adequate salt-retaining effect by the kidneys and a decrease in with hydrocortisone (see Treating gastric acid production may lead to patients with adrenal insufficiency).3 anorexia and weight loss.1–3 Pain in adrenal insufficiency, re- Diminished aldosterone secretion lated to fluid and electrolyte imbal- triggers fluid and electrolyte imbal- ances, can occur in the abdomen, ances. Sodium and water excretion lower back, and legs. Over-the- is increased, with resultant hypona- counter (OTC) medications such as tremia and hypovolemia. Potassium acetaminophen help manage pain; excretion is reduced, causing hyper- patients also may need adjustments kalemia. Potassium retention also to the dosages of glucocorticoid facilitates reabsorption of hydrogen replacement drugs. ions within the renal tubules, which Adrenal crisis requires immediate may cause acidosis. The adrenal glands treatment to maintain essential met- Acute adrenal crisis (also called are highly vascular, abolic functions. Follow the “5 S’s” Addisonian crisis) is a life-threatening tent-shaped organs for management: complication in which adrenal insuf- located on top 1. salt replacement ficiency manifests without warning, of the kidneys. 2. sugar (dextrose) replacement often due to a stressful event such as 3. steroid replacement surgery, trauma, or infection. The 4. support of physiologic functions. patient’s need for cortisol and aldos- 5. search for and treat any identified terone is greater than the body’s sup- sodium. Potassium and blood urea cause.3 ply, so hyponatremia, hypovolemia, nitrogen (BUN) levels are elevated. Replace extracellular fluid volume and hyperkalemia progress rapidly, Patients with primary adrenal insuf- with 5% dextrose and 0.9% sodium putting the patient at risk for car- ficiency also have an elevated ACTH chloride solution as prescribed. diovascular collapse (more on level and an elevated eosinophil Monitor for electrolyte abnormali- this later).1,3 count secondary to decreased levels ties; hyperkalemia is often present of circulating cortisol. and may be treated with I.V. insulin Recognizing adrenal The most conclusive diagnostic and glucose to shift potassium into insufficiency test for adrenal insufficiency is an the cells. Administer I.V. hydrocorti- Lab results show decreased serum ACTH stimulation test, performed sone or dexamethasone, followed levels of cortisol, fasting glucose, and by administering I.V. ACTH and by continued use of hydrocortisone assessing plasma cortisol levels at for long-term treatment, as pre- Lab findings for