Ch. 42 Adrenal Disorders (exam 3)

Hypercortisolism signs and symptoms

- emotional disturbance - enlarged sella turcica - moon face - osteoporosis - cardiac hypertrophy - breast atrophy - adrenal tumor or hyperplasia - obesity - thin, wrinkled skin - abdominal striae - amenorrhea - decreased muscle mass - purpura - Skin ulcers

Adrenal Cortex Hyperfunction

- more common in females than males - may be d/t excessive secretion of glucocorticoids or excessive secretion of aldosterone - it is characterized are primary, secondary, or tertiary

Adrenal Cortical Insufficiency

- more common in women - peak incidence age 30-50 - results from destruction of the adrenal glands (d/t addison's disease) - decreased secretion of ACTH from ant. pit gland (secondary insufficiency) or dysfunction of the adrenal gland is most common cause of primary adrenal insufficiency

5. The nurse monitors for which complication in Ms. Davis secondary to her hypercortisolism? A. Osteoporosis B. Hypoglycemia C. Muscle loss D. Hyperkalemia

A Osteoporosis may develop relative to the effects of cortisol on bone density and can increase the risk of pathologic fractures. Patients with hypercortisolism have hyperglycemia, not hypoglycemia, and hypokalemia. Muscle loss is more associated with adrenal insufficiency, not excessive cortisol.

2. The nurse assesses for which clinical manifestations in the patient admitted with primary hypercortisolism? (Select all that apply.) A. Elevated serum glucose B. Elevated serum potassium C. Elevated urine-specific gravity D. Elevated blood pressure E. Elevated temperature

A and D The clinical manifestations of hypercortisolism are directly related to hypersecretion of cortisol and include hyperglycemia, fluid retention, hypokalemia, abnormal fat distribution, and decreased muscle mass. The maldistribution of fats and changes in muscle are related to the effects that glucocorticoids have on fat and protein metabolism.

actions for pheochromocytoma

Administer sodium nitroprusside (Nipride) — Quickly decreases blood pressure through direct action on blood vessels, leading to peripheral vasodilation Administer alpha-adrenergic blocking agents — This decreases blood pressure by blocking the alpha-adrenergic effects on blood vessels that lead to vasoconstriction. The blocking action results in vasodilation. Administer beta-adrenergic blocking agents — Beta-adrenergic agents lead to increased chronotropic (rate) and inotropic (force) effects on the heart. Beta-adrenergic blocking agents decrease the heart rate and force of contraction. Bed rest with head of bed elevated — Bed rest decreases secretion of catecholamines and elevating the head of the bed facilitates orthostatic hypotension. Maintain calm, quiet environment — Because of increased circulating levels of catecholamines, it is important to minimize stimuli that could potentially cause stress and additional catecholamine secretion. Administer glucocorticoid the morning of surgery for adrenalectomy — Minimizes the risk of adrenal insufficiency postoperatively because of manipulation of adrenal, particularly in patients requiring bilateral adrenalectomy.

Secondary insufficiency

Adrenal insufficiency may result from destruction of the adrenal glands (primary insufficiency or Addison's disease), decreased secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland

surgical management of pheochromocytoma

Adrenalectomy is the definitive treatment for pheochromocytoma, and the goals include complete tumor resection, minimal tumor manipulation, and adequate exposure of the adrenal gland to avoid injury to other organs. There are several approaches for adrenalectomy, including open anterior transabdominal, open thoracoabdominal, open posterior or lateral retroperitoneal, lateral transabdominal laparoscopic, and posterior retroperitoneal laparoscopic approaches

4. The nurse questions which intervention in the patient diagnosed with hypercortisolism? A. Limit salt intake B. Limit foods containing potassium C. Increase weight-bearing exercises D. Avoid use of skin tape

B Hypokalemia develops in the patient with hypercortisolism as cortisol leads to loss of potassium and sodium retention. There would be no rationale in limiting potassium in this patient at risk for hypokalemia.

1. The nurse correlates primary hypercortisolism to dysfunction of which gland? A. Hypothalamus B. Anterior pituitary gland C. Adrenal cortex D. Adrenal medulla

C Cortisol is the primary glucocorticoid released from the adrenal cortex. Primary endocrine disorders are associated with the endocrine gland, and in this example, the adrenal cortex. Secondary endocrine disorders are related to anterior pituitary gland dysfunction, and tertiary disorders are related to hypothalamic dysfunction. The adrenal medulla secretes epinephrine and norepinephrine

teachings for pheochromocytoma

Clinical manifestations of adrenal insufficiency — In patients with bilateral adrenalectomy, lifelong cortisol replacement is required. The patient is at risk of adrenal insufficiency, especially during times of physiological or emotional stress. Postoperative teaching related to adrenalectomy — The patient should monitor body temperature as well as surgical site for signs of infection

hyperaldosteronism

Conn's syndrome Because the primary actions of aldosterone are sodium and water reabsorption and potassium excretion, hypertension and hypokalemia develop. The incidence of hyperaldosteronism is significantly greater in African Americans than in Caucasians. There is an autosomal dominant pattern of inheritance for primary hyperaldosteronism, with females more at risk than males. - hyperfunction of adrenal cortex

3. Which of the following patients is at greatest risk for primary hypercortisolism? A. A 65-year-old male B. A 56-year-old female C. A 44-year-old male D. A 28-year-old female

D Females are five times more likely to develop primary hypercortisolism, and the peak incidence of hypersecreting tumors of the adrenal and pituitary glands is in the 25- to 40-year age range.

evaluating care outcomes pheochromocytoma

Definitive treatment of pheochromocytoma with adrenalectomy results in complete resolution of this disease process. Because there is the possibility of incomplete resection of the pheochromocytoma or recurrence in patients with a family history of this disorder, patients need to have periodic checks of their blood pressure. Only patients with bilateral tumors requiring bilateral adrenalectomy require lifelong cortisol replacement.

nursing diagnosis of adrenal cortical insufficiency

Fluid volume deficit associated with sodium and water losses secondary to lack of aldosterone and cortisol Risk for unstable blood glucose level associated with decreased cortisol secretion from the adrenal cortex Risk for decreased cardiac output associated with acute adrenal crisis (loss of sodium and water) Body image disturbance associated with hyperpigmentation secondary to increased secretion of MSH from the anterior pituitary gland

Adrenal Cortex Hyperfunction nursing interventions

Fluid volume excess associated with increased sodium and water reabsorption secondary to excess glucocorticoid secretion Body image disturbance associated with development of truncal obesity and fat deposition secondary to excess glucocorticoid secretion Risk for infection related to associated with immunosuppression Deficient knowledge associated with diagnosis of hypercortisolism Hyperaldosteronism: Fluid volume excess associated with increased sodium and water reabsorption secondary to excess aldosterone secretion Risk for decreased cardiac output associated with cardiac dysrhythmias secondary to hypokalemia Deficient knowledge associated with management of hyperaldosteronism Vital signs — Suppressed immune function secondary to hypercortisolism increases the risk of infection. Small increases in body temperature may be significant, and signs of infection and may be masked because of immune suppression. Blood pressure and heart rate may increase secondary to fluid retention. Intake and output — Monitoring is important to evaluate trends once treatment has been started. Urine output should increase and signs of fluid overload should decrease if treatment is effective. Serum glucose, potassium — Glucose levels rise secondary to increased secretion of glucocorticoid. Potassium levels also fall secondary to increased excretion via the kidneys secondary to glucocorticoid and mineralocorticoid activity. Daily weight — Weight gain occurs secondary to fluid retention secondary to sodium and water reabsorption. Peripheral edema may develop. Skin — Thinning skin and increased friability develop secondary to excess cortisol. Fat distribution — Actions of glucocorticoid affect fat metabolism, leading to maldistribution of fat including truncal obesity, moon face, and buffalo hump. Muscle mass — Muscle atrophy develops secondary to altered protein metabolism. Wound healing — Delayed wound healing occurs associated with the suppressed inflammatory response. Administer medications that interfere with production/secretion of cortisol — Decreases secretion of cortisol Head of bed elevated 45 degrees — Decreases work of breathing that may develop secondary to fluid retention Turn patient frequently and protect skin from injury — Thinning of skin along with increased friability of skin accompanied by fluid retention increases the chances of skin injury caused by pressure or friction.

Cushing's syndrome is d/t _____ of the adrenal cortex

Hyperfunction. - it is a condition caused by excessive hormone production from an anterior pituitary tumor (70%) producing excessive ACTH or excess hormone secretion from a primary tumor of the adrenal cortex (15%). - Approximately 15% of cases of hyperfunction are related to ectopic tumors, usually in the lung, that secrete ACTH. Cushing's syndrome is a more broad term and may be used to describe an excess of hormone production (CRH, ACTH, glucocorticoids) or administration of exogenous corticosteroid medications. Despite the etiology, the clinical presentations of hypercortisolism are similar. Females are five times more likely to develop this disorder, and the peak incidence of hypersecreting tumors of the adrenal and pituitary glands is in the 25- to 40-year age range.

primary insufficiency

Nonspecific autoimmune destruction of the adrenal gland is the most common cause of primary adrenal insufficiency Other causes of primary adrenal insufficiency include infectious, cancerous, and traumatic processes that lead to direct insults to the adrenal cortex. Secondary and tertiary adrenal insufficiencies are related to disorders of the anterior pituitary gland and hypothalamus, respectively. Despite the etiology, the clinical presentations of adrenal insufficiency are similar. Females are most often affected by adrenal insufficiency, and it has a peaked incidence in people 30 to 50 years of age.

teachings for Adrenal Cortex Hyperfunction

Overview of disease process — It is important that the patient (and family) is able to detect early signs of both hypercortisolism and adrenal insufficiency. Importance of taking prescribed medications — Medications that interfere with cortisol production are key to disease management. Modify salt in diet as directed by provider — Excessive salt intake may further exacerbate fluid retention.

Pheochromocytoma

Pheochromocytomas are rare catecholamine-secreting tumors of the adrenal medulla and, in 50% of cases, are diagnosed only on autopsy. Because of excessive catecholamine (epinephrine and norepinephrine) secretion, pheochromocytomas may precipitate life-threatening hypertension or cardiac arrhythmias, leading to sudden death. Occurring in all races, the incidence is higher in Caucasians. In relation to age, the peak incidence is in people 30 to 50 years of age. It is estimated that 25% of pheochromocytomas are familial and specific gene mutations. There are approximately 1,000 cases of pheochromocytoma diagnosed in the United States annually.

surgical management of adrenal cortex hyperfunction

Surgical management of hypercortisolism is based on the etiology of the disorder. If the etiology is a pituitary tumor, a transsphenoidal hypophysectomy is performed. With hypersecreting tumors of the adrenal cortex, an adrenalectomy (removal of the adrenal gland) may be indicated (presented later in this chapter). Radiation therapy, including stereotactic radiosurgery of the pituitary gland, may also be used in the management of tumors of the pituitary gland (see Evidence-Based Practice).

teaching for adrenal cortical insufficiency

Take oral hormone replacement daily — Adrenal cortex replacement is required to maintain fluid balance and normal glucose levels. Wear medical alert bracelet at all times — Wearing the medical alert bracelet reduces time to definitive treatment in an emergency situation. Clinical manifestations of adrenal insufficiency — It is important that the patient (and family) is able to detect early signs of adrenal insufficiency because it can deteriorate to adrenal crisis, which is a life-threatening emergency. Signs of corticosteroid excess — Over-replacement of glucocorticoids results in adverse effects including weight gain and osteoporosis

general signs of adrenal cortex hyperfunction

The clinical manifestations observed in the patient with adrenal cortex hyperfunction are directly related to elevated circulating levels of cortisol or aldosterone. Common findings in patients with hypercortisolism include: Hypertension Hyperglycemia Dependent edema Thin, friable skin Fat maldistribution (truncal obesity, "moon face," and "buffalo hump") (Fig. 42.2) Loss of bone density Decreased inflammatory process l Increased risk of infection Patients with hyperaldosteronism present with the following manifestations: Hypertension Hypernatremia Hypokalemia Headache

general signs and symptoms of adrenal cortical insufficiency

The clinical manifestations of adrenal insufficiency, whether acute or chronic, are directly related to the actions of the adrenal cortex hormones. The nurses correlates adrenal insufficiency with the following clinical manifestations. Hypotension associated with loss of sodium (hyponatremia) and water Hypoglycemia associated with decreased cortisol Hyperkalemia associated with decreased aldosterone Muscular weakness associated wit hdecreased glucocorticoid and hyperkalemia Abdominal pain, nausea, weight loss Emotional lability

assessment and analysis for pheochromocytoma

The clinical presentation of pheochromocytoma is directly related to the effects of increased levels of circulating epinephrine and norepinephrine: Hypertension (often paroxysmal attacks) Tachycardia Hyperglycemia Pounding headaches

nursing interventions for adrenal cortical insufficiency

Vital signs — Decreased blood pressure occurs secondary to lack of aldosterone, leading to loss of sodium and water. While blood pressure decreases, there is a compensatory increase in pulse rate. Irregular heart rate may also be associated with hyperkalemia. Monitor intake and output — Fluid loss occurs secondary to lack of mineralocorticoid and glucocorticoid, leading to loss of sodium followed by loss of water through the kidneys. Serum sodium, glucose, and potassium — Decreased gluconeogenesis occurs because of lack of glucocorticoid. Lack of glucocorticoid and mineralocorticoid leads to loss of sodium and water and retention of potassium. Hematocrit and blood urea nitrogen (BUN) — Fluid losses lead to hemoconcentration that may increase hematocrit and serum BUN levels. Serum cortisol levels — Random serum cortisol levels of less than 3 mcg/dL or levels of less than 13 mcg/dL with a corticotropic stimulation test suggest adrenal insufficiency. Ensure vascular access for administration of IV fluids containing sodium and glucose — Loss of water occurs secondary to increased excretion of sodium (direct action of aldosterone). Initiating IV access is complicated with hypovolemia. Administer corticosteroid — Definitive treatment of acute adrenal insufficiency (adrenal crisis) is administration of IV cortisone. Maintain safety precautions such as placing the patient's bed in the lowest position and always providing assistance when the patient is getting out of bed — Postural hypotension may develop secondary to fluid losses, placing the patient at greater risk of falls.

nursing interventions of pheochromocytoma

Vital signs — Hypertension and tachycardia develop secondary to excessive circulating catecholamines from pheochromocytoma. In the patient who undergoes adrenalectomy, the patient may develop signs of hypovolemia and shock secondary to hemorrhage. Cardiac monitoring — The patient is at risk of tachydysrhythmias secondary to elevated catecholamines. Headache — Pounding headaches develop secondary to hypertension. Plasma catecholamine levels — Increased secretion of catecholamines from the tumor leads to elevated free plasma levels. Plasma and catecholamine metabolite measurements (VMA) — Elevated levels of catecholamines result in increased levels of catecholamine metabolites.

kerfuffle

a commotion or fuss, especially one caused by conflicting views

Darkened, bronzed hyperpigmentation results from what?

an increased secretion of ACTH d/t to adrenal insufficiency

primary hypercortisolism

disease of the adrenal cortex, causing hyper or hypo - example is cushings syndrome

tertiary insufficiency

dysfunction of the hypothalamus

secondary hypercortisolism

hyperfunction of anterior pituitary ACTH-secreting cells

tertiary hypercortisolism

hypothalamic dysfunction or injury

treatment for pheochromocytoma

•Bedrest •Elevate H O B •Cardiac monitor Patients presenting with signs of hypertension, tachycardia, and other clinical manifestations of pheochromocytoma require bedrest with the head of the bed elevated, usually in a critical care setting. The patient is placed on a cardiac monitor to assess for cardiac dysrhythmias.

Pathophysiology of Pheochromocytoma

•Catecholamine-secreting tumors •Vasoconstriction, increased heart rate, increased stroke volume, rise in systolic blood pressure, widened pulse pressure, hyperglycemia Pheochromocytomas are catecholamine-secreting tumors of the adrenal medulla and are usually unilateral. The release of epinephrine and norepinephrine is typically paradoxical, rather than continuous, and leads to vasoconstriction, increased heart rate, increased stroke volume leading to a rise in systolic blood pressure and a widening of pulse pressure. Catecholamine release also stimulates gluconeogenesis, resulting in hyperglycemia.

Diagnosis of pheochromocytoma

•Clinical presentation •Laboratory studies •Imaging studies The classic presentation of pheochromocytoma is marked by a sudden elevation of blood pressure accompanied by other clinical manifestations of catecholamine excess. This clinical presentation, along with specific diagnostic studies, assists in making a definitive diagnosis. Diagnostic assessments for this disorder include measurements of urine and plasma levels of catecholamines and catecholamine metabolites as well as imaging studies. Direct measurements of plasma catecholamines require specific patient preparation to prevent elevations of circulating catecholamines. The patient is placed supine and rests for 30 minutes prior to the test. Additionally, small IV catheters are placed approximately 30 minutes prior to the actual collection of the blood samples. Catecholamine metabolites such as metanephrine and vanillylmandelic acid (VMA) and free catecholamines are also measured in urine. These tests require 24-hour urine collections. Preparation for these tests requires the patient to avoid specific foods, beverages, and medications prior to and during the urine collection. The patient is instructed to avoid bananas, chocolate, vanilla, and tea or coffee (including decaffeinated varieties) because these are high in amines and can lead to a false elevation of VMA. Imaging studies, including CT or MRI scans, are also indicated in the diagnostic work-up for pheochromocytomas. Data from these studies determine whether tumors are unilateral or bilateral. Additionally, imaging data are very important in guiding the surgeon performing the adrenalectomy.

diagnosis for adrenal cortex hyperfunction

•Cortisol levels •Suppression tests •Serum electrolytes Diagnostic evaluation of hypercortisolism includes assessment of cortisol levels, results of suppression tests, and serum electrolytes. Because aldosterone secretion results in both sodium and water reabsorption, there may not be an increase in serum sodium (secondary to water reabsorption); however, the patient does present with hyperglycemia (secondary to glucocorticoid activity) and hypokalemia. Measurement of urinary free cortisol is used as an initial screening tool because it measures urine cortisol during a 24-hour period. The overnight dexamethasone suppression test is another tool to evaluate hypercortisolism, specifically whether the administration of exogenous glucocorticoid (dexamethasone) inhibits the secretion of ACTH that, in turn, decreases stimulation of cortisol release. In this diagnostic study, dexamethasone, 1 mg, is administered at 11 p.m. followed by the collection of a serum cortisol level at 8 a.m. the next morning. The results are based on whether suppression of cortisol secretion occurs secondary to the administration of exogenous glucocorticoid. If the morning level is less than 2 to 3 mg/dL, normal functioning of the hypothalamic-pituitary-adrenal axis is determined. The ACTH level can also be measured, and changes may be secondary to changes in the secretion of CRH from the hypothalamus.

complications of adrenal cortex hyperfunction

•Damage to heart, vascular, kidneys, eyes •Cardiac dysrhythmias Complications of hyperaldosteronism are primarily related to hypertension and severe hypokalemia. Untreated hypertension leads to damage to other organs including the heart, vasculature, kidneys, and eyes. Additionally, uncontrolled high blood pressure increases the risk for acute myocardial infarction and acute stroke (cerebrovascular accident). Cardiac dysrhythmias are associated with severe hypokalemia.

signs and symptoms of adrenal cortical insufficiency

•Darkened, bronzed hyperpigmentation •Weakness •Weight loss •Fatigue •Nausea •Abdominal pain •Gastroenteritis •Emotional lability Clinical manifestations of adrenal insufficiency usually present after 90% of the adrenal cortex is destroyed or nonfunctional. While the circulating levels of cortisol and aldosterone fall, the hypothalamus and anterior pituitary gland increase secretion of CRH and ACTH, respectively. Because melanocyte-stimulating hormone (MSH) and ACTH share a progenitor (ancestor) hormone, there is an associated increase in secretion of MSH, leading to a darkened, bronzed hyperpigmentation that accompanies the increased secretion of ACTH. Secondary to the decreased secretion of cortisol and aldosterone, the patient presents with weakness, weight loss, fatigue, nausea, abdominal pain, gastroenteritis, and emotional lability. Changes in mood include irritability, depression, and inability to concentrate. Hyperpigmentation of the skin and mucous membranes and decreased pubic and axillary hair (secondary to decreased secretion of sex hormones) are also observed. As the loss of sodium and water continues, the patient may develop dehydration and hypotension.

pathophysiology of adrenal cortical insufficiency

•Decreased secretion of corticotropin-releasing hormone •Decreased secretion A C T H from anterior pituitary •Decreased secretion of glucocorticoids and mineralocorticoids from adrenal cortex The pathophysiology of adrenal insufficiency may be associated with decreased secretion of corticotropin-releasing hormone (CRH) from the hypothalamus, decreased secretion of ACTH from the anterior pituitary gland, or decreased secretion of glucocorticoids and mineralocorticoids from the adrenal cortex. Patients who are prescribed exogenous corticosteroids for longer than 2 weeks are at risk for acute adrenal insufficiency (acute adrenal crisis) if the medications are abruptly discontinued

pathophysiology of Adrenal Cortex

•Excessive circulating glucocorticoid •Excessive secretion of A C T H Excessive circulating glucocorticoid (cortisol) is the pathophysiological process associated with primary hypercortisolism. Excessive secretion of ACTH from the anterior pituitary gland leads to hypercortisolism through its effects on the adrenal cortex.

signs and symptoms of hyperfunction of adrenal cortex

•Hyperglycemia •Fluid retention •Hypokalemia •Abnormal fat distribution •Decreased muscle mass The clinical manifestations of adrenal cortex hyperfunction are directly related to hypersecretion of these hormones and include hyperglycemia, fluid retention, hypokalemia, abnormal fat distribution, and decreased muscle mass. The maldistribution of fats and changes in muscle are related to the effects that glucocorticoids have on fat and protein metabolism. In female patients, clinical manifestations include virilization (male sexual characteristics developing in females), breast atrophy, vocal changes (deepening), and amenorrhea. Overproduction of cortisol also affects the immune system by decreasing inflammatory and immune responses. Lymphocytes are also destroyed secondary to high levels of circulating cortisol, further placing the patient at risk for infection.

complications of adrenal cortical insufficiency

•Hypovolemia •Hypotension •Hyperkalemia •Hypoglycemia Acute adrenal insufficiency, or adrenal crisis, is a life-threatening emergency that leads to severe hypovolemia and hypotension. Risk factors for adrenal crisis are seen in patients who have underlying adrenal hypofunction and who undergo stressful events such as trauma, surgery, and infections. Because of the decrease in aldosterone and cortisol, the patient loses sodium accompanied by fluid loss. The patient is also at risk for hyperkalemia and hypoglycemia associated with lack of both mineralocorticoids and glucocorticoids. Patients with primary adrenal insufficiency require additional doses of glucocorticoid during periods of stress such as surgery, trauma, or infection.

Medications for pheochromocytoma

•Lower blood pressure •Smooth muscle relaxants •Calcium channel blockers Pharmacological management focuses on quickly lowering the blood pressure and includes alpha-adrenergic blocking agents or smooth muscle relaxants. Other medications that may be administered include beta-adrenergic blocking agents and calcium channel blockers to decrease blood pressure and heart rate.

evaluating care outcomes

•Normal adrenal cortex function •Vital signs in normal limits •Increased energy •Stable weight •Emotional stability Patients with adrenal insufficiency can achieve normal adrenal cortex function with treatment with exogenous corticosteroids. Positive outcomes include vital signs within normal limits, increased energy, stable weight, and emotional stability. During periods of stress, such as invasive procedures, an increase in exogenous corticosteroids is often necessary. It is important for all healthcare providers to be aware of adrenal insufficiency, particularly when prescribing medications such as sedatives, narcotics, or anesthetic agents. The patient and family should be knowledgeable about the clinical manifestations of adrenal insufficiency and what changes require immediate reporting to the healthcare provider

treatment of adrenal cortex hyperfunction

•Prevent complications •Medications that suppress A C T H and glucocorticoid production Medical management of hypercortisolism focuses on preventing complications associated with fluid overload, changes in immune status, changes in skin integrity, and changes in body structure. Medications that interfere with ACTH and glucocorticoid production are used in the treatment of hypercortisolism. Aminoglutethimide is an example of a medication that interferes with cortisol production in the adrenal cortex, and cyproheptadine impacts ACTH production. With both types of medications, the nurse must monitor for signs of adrenal suppression including hypoglycemia and hyponatremia. Pasireotide (Signifor), a subcutaneous somatostatin analog, is a medication used to inhibit release of corticotropin in patients with Cushing's disease secondary to a pituitary adenoma.

medications for adrenal Cortical Insufficiency

•Replacement of cortisol •Glucocorticoids Replacement of cortisol is the definitive treatment for adrenal insufficiency. Patients presenting with acute adrenal insufficiency require emergency stabilization with IV fluids and glucose, along with IV administration of glucocorticoids (cortisol), such as 50 to 100 mg of hydrocortisone sodium succinate (Solu-Cortef) or 4 to 12 mg of dexamethasone (Decadron). One of the advantages of hydrocortisone is that it has both glucocorticoid and mineralocorticoid actions. The patient requires close monitoring, including frequent assessments of vital signs, level of consciousness, and serum sodium, glucose, and potassium levels to ensure an adequate dosage of cortisol. In patients presenting with hyperkalemia, treatment with potassium binding or excreting agents (Kayexalate) are indicated.

nursing diagnosis for pheochromocytoma

•Risk for injury •Acute pain Risk for injury: Cerebrovascular hemorrhage related to severe hypertension Acute pain: Headache related to increased levels of circulating catecholamines secondary to the hypersecreting tumor (pheochromocytoma) Risk for injury: Postoperative hemorrhage related to adrenalectomy

signs and symptoms of pheochromocytoma

•Tachycardia •Hypertension •Severe headaches •Palpitations •Hyperhidrosis •Hypermetabolism •Hyperglycemia Clinical manifestations of this disorder are associated with the systematic actions of epinephrine and norepinephrine and include tachycardia, hypertension, severe headaches, palpitations, hyperhidrosis (excessive sweating), hypermetabolism, and hyperglycemia. The severity of attacks correlates to the amount of catecholamine release. Paroxysmal (sudden-onset) hypertension is seen in some patients, with blood pressure elevations in excess of 250/140 mm Hg, posing a life-threatening emergency.

evaluating care outcomes for adrenal cortex hyperfunction

•Treat etiology of disorder •Maintain corticosteroid therapy •Stable vital signs and fluid status Patients with hypercortisolism are usually best managed once the etiology of the disorder is determined. If the etiology is a hypersecreting tumor of the pituitary gland or adrenal cortex, surgical intervention (transsphenoidal hypophysectomy, adrenalectomy, or stereotactic radiosurgery) is indicated. The patient should be closely monitored postoperatively and may require lifelong corticosteroid replacement on the basis of the surgical outcome. Stable vital signs and fluid volume status, serum electrolytes within normal limits, and intact skin are expected outcomes with treatment of hyperfunction of the adrenal cortex.