Adrenal Glands

Cushing’s Syndrome

 Hypersecretion by adrenal cortex results in hypercortisolism

o Cushing’s disease
 Pituitary Cushing’s disease
 Adrenal Cushing’s disease
o Cushing’s syndrome

Etiology

Cushing’s Disease (Endogenous secretion) Cushing’s Syndrome (Exogenous Secretion)

 Pituitary adeonoma  Therapeutic use of ACTH or
 Adrenal adenoma or carcinoma glucocorticoids – most commonly for the
 Bilateral adrenal hyperplasia treatment of
 Malignancies o Asthma
o Lung o Autoimmune disorders
o GI tract o Organ transplantation
o Pancreas o Cancer chemotherapy
o Allergic responses
o Chronic fibrosis

Cushing’s Disease

Clinical Manifestations

General appearance  Fat redistribution (moon face, buffalo

hump, truncal obesity)
 Weight gain
 Cardiac changes  Na, H2O retention (hypervolemia, HTN,
edema)
Musculoskeletal changes  Nitrogen depletion, mineral loss (↓
muscle mass and strength, osteoporosis,
back pain)
Glucose metabolism  Hyperglycemia
Immune changes  ↑ risk for infection
Skin changes  ↑ blood vessel fragility (bruising, thin or
translucent skin, poor wound healing,
striae, acne, hirsutism)

Clinical Manifestations

Diagnostic Studies

 ↑ 24-hr urinary free cortisol level

 ↑ urine 17-ketosteroid measurement
 Midnight plasma control and late-night salivary cortisol measurements
o Cortisol level >50 nmol/L
 Low-dose dexamethasone suppression test
o ↑ cortisol level
 Additional laboratory findings that accompany hypercortisolism
o ↑ blood glucose and serum sodium levels
o ↓ serum potassium and calcium levels
o ↓ lymphocyte count
 CT scan
 MRI
 Subjective data
 o Past health history – e.g, pituitary tumor, malignancies (lung, GI tract, pancreas),
frequent infections
o Medications – e.g., use of corticosteroids
o Functional health patterns – e.g., changes in sleep patterns, muscle weakness, back and
joint pain, emotional lability
 Objective data
o General appearance
o Mood swings, irritability
o Skin, cardiac, musculoskeletal changes
o Immune changes
 Expected inflammatory manifestations may not be present
o Sleep difficulties, fatigue
o Abnormal diagnostic findings

Nursing Diagnoses and Planning

 Nursing diagnoses
o Disturbed body image
o Impaired skin integrity
o Risk for injury
o Potential for infection
 Planning: Overall goals – the patient will
o Maintain positive self-image
o Maintain intact skin
o Avoid injuries
o Remain free from infection
o Have no complications

Collaborative Care

 Normalization of hormone secretion

 Treatment depends on cause
o Surgical removal or irradiation of pituitary adenoma
o Adrenalectomy for adrenal tumors or hyperplasia
o Removal of ACTH-secreting tumors
 If cause is iatrogenic
o Discontinue therapy gradually
o Decrease dose
 Dose must be tapered gradually
o Convert to an alternate-day regiment
 Nonsurgical management
o Monitoring for indicators of increased fluid overload
 Pulmonary edema can occur very quickly
 Rapid weight gain is the best indicator of fluid retention and overload
 Preventing injury
o Risk for skin breakdown in patients with fluid overload and dependent edema
 o Avoidance of activities that can result in trauma
 ↑ risk of bleeding because of blood vessel fragility
 Pathologic fractures are possible
 Monitoring blood glucose
 Drug therapy that provide temporary ↓ in cortisol production
o Ketoconazole
o Mitotane
o Metyrapone
o Aminoglutethimide
 Drug therapy for GI bleeding
o Antacids
o H2-receptor blockers
o Proton pump inhibitors
o Avoidance of NSAIDs and drugs that contain ASA
 Diet
o Fluid and sodium restriction to control fluid volume
o Calcium and vitamin D
o Avoidance of alcohol, caffeine, fasting, smoking
 Infection prevention
o Hand hygiene
o Assessmentfor possible infection
o Temperature, WBC, ANC monitoring
o Skin care
o Pulmonary hygiene
o Appropriate vaccinations
o Avoiding crowds
 Radiation therapy
o Not always effective and often destroys normal tissue
o Patient may have neurologic changes and skin dryness, redness, flushing, or alopecia at
radiation site
 Emotional support
o Changes in appearance can be distressing
o Physical changes and emotional lability will resolve when hormone levels return to
normal
 Surgical management
o Hypophysectomy
 Adrenal hyperfunction is due to ↑ pituitary secretion ACTH
o Adrenalectomy
 Hypercortisolism caused by adrenal tumors
o Preop care
 Correction of electrolyte imbalances
 Cardiac and BP monitoring
 Glycemic control
 Glucocorticoid administration
  Removal of tumor results in sudden drop in cortisol levels
 High protein diet
 Preop teaching
o Postop care
 Ongoing monitoring of VS, fluid balance, electrolyte levels, and manifestations
of shock and bleeding
 Acute adrenal insufficiency if corticosteroid tapered too quickly
 Infection prevention
 Delayed wound healing
 Emboli prevention
 Bedrest until BP stabilized
 Morning urine samples for cortisol measurement
 Unilateral adrenalectomy  hormone replacement until remaining adrenal
gland ↑ hormone production
 Bilateral adrenalectomy  lifelong hormone replacement
 Ambulatory and home care
o Wear MedicAlert bracelet at all times
o Avoid exposure to extremes of temperature, infection and stress
o Teach how to adjust medication and when to call health care provider
o Encourage compliance with lifetime replacement therapy

Health Promotion

 Identify patients at risk for Cushing’s syndrome

o Long-term exogenous cortisol therapy is major risk factor
 Teach patients about medication use and to monitor for side effects

Evaluation

 Positive body image

 Intact skin
 No complications

Hyperaldosteronism

 Adrenal gland releases too much of the hormone aldosterone

o Primary hyperaldosteronism (Conn’s syndrome)
 Solitary adrenocortical adenoma
 Genetic link
o Secondary hyperaldosteronism
 Renal artery stenosis
 Renin-secreting tumors
 Chronic kidney disease
 ↑ aldosterone levels  sodium retention with potassium and hydrogen ion excretion  ↑
blood volume
 HTN with hypokalemia alkalosis = hallmark
  Clinical manifestations
o Sodium retention
 H/A, HTN, no peripheral edema
o Hypokalemia
 Cardiac dysrhythmias
 Muscle weakness, fatigue
 Metabolic alkalosis  tetany
 Diagnostic studies
o Laboratory tests
 ↑ serum sodium, ↓ serum potassium
 ↑ aldosterone level, ↓ plasma renin level
 Metabolic alkalemia
 ↑ plasma 18-hydroxycorticosterone level
o Urine has low specific gravity and high aldosterone levels
o X-ray, CT, MRI
 Collaborative care
o Adrenalectomy to remove adenoma
 Preop
 Potassium-sparing diuretics
 Antihypertensives
 Oral potassium supplements
 Sodium restriction
o Bilateral adrenal hyperplasia
 Potassium-sparing diuretic to block aldosterone synthesis
 Calcium channel blockers to ↓ BP
 Dexamethasone to ↓ hyperplasia
o Careful assessment
 Fluid and electrolyte balance
 Cardiovascular status
o Patient teaching
 Medications and side effects
 Sign and symptoms of hypokalemia and hyperkalemia
 Frequent monitoring

Pheochromocytoma

 Rare, catecholamine-secreting tumor that arises in the adrenal medulla

o Tumor produce, store and release epinephrine and norepinephrine  life-threatening
HTN
o Unknown cause but some occur with inherited disorders
 Slightly more often in women
 Most commonly between 40 and 60 years of age
 Clinical manifestations
o Intermitted episdes of HTN
o Severe H/A, palpitations
 o Profuse diaphoresis, flushing
o Apprehension, impending sense of doom
o Chest or abdominal pain with N/V
o Heat intolerance, weight loss, tremors
 Precipitating factors of HTN crisis in patients with pheochromocytoma
o ↑ abdominal pressure (e.g., vigorous abdominal palpation), defecation
o Drugs
 Tricyclic antidepressants, droperidol, metoclopramide, phenothiazide, glucagon,
naloxone
o Food or beverages high in tyramine
 E.g., aged cheese, red wine
 Diagnostic studies
o 24-hr urine collection for vanillymandelic acids, mentanephrine, catecholamines
 ↑ in presence of pheochromocytoma
o Clonidine suppression test
o CT scan, MRI
 Collaborative care
o Blood pressure monitoring
 Cuff consistently on same arm
 BP with patient lying and standing
o Identification of precipitating factors
 No smoking, drinking of caffeine-containing beverages or changing positions
suddenly
o Calm, restful environment for the patient with severe H/A
 Private, darkened room to promote rest
 If possible, avoid interruptions when patient sleeping
 Limitation of activity
 Collaborative care: Surgical management
o Preop
 Hydration
 Stabilization of BP
 Adrenergic blocking agents – e.g., phenoxybenzamine
o Intraop
 Short-acting alpha-adrenergic blockers
 Anesthetic agents and touching of tumor during surgery can cause
catecholamine release
o Postop
 Nursing care similar to that for the patient who has undergone adrenalectomy
 Collaborative care for inoperable tumor
o Alpha-adrenergic and beta-adrenergic blocking agents
 Tumor do not respond well to chemo and radiation
o Patient teaching
 Self-measurement of BP