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Interventions for Clients

with Pituitary and Adrenal
Gland Problems
 Hormones secreted from the anterior pituitary gland
regulate growth, metabolism, and sexual
development. These functions are affected when the
pituitary gland secretes too much or too little of one
or more hormones

 The posterior pituitary gland secretes vasopressin
(antidiuretic hormone [ADH]). Dysfunction of the
posterior pituitary gland results in fluid and electrolyte
imbalance

 The adrenal gland produces and secretes hormones
that influence homeostasis and are life sustaining
DISORDERS OF THE PITUITARY GLAND
 The anterior pituitary gland
(adenohypophysis) controls growth,
metabolic activity, and sexual development
through the actions of the following hormones:
 Growth hormone (GH; somatotropin)
 Prolactin (PRL)
 Thyrotropin (thyroid-stimulating hormone [TSH])
 Corticotropin (adrenocorticotropic hormone [ACTH])
 Follicle-stimulating hormone (FSH)
 Luteinizing hormone (LH)
 Melanocyte-stimulating hormone (MSH)
DISORDERS OF THE PITUITARY GLAND
 Disorders of hormones secreted by the anterior
pituitary gland can result from problems arising
within the anterior pituitary gland itself
(primary pituitary dysfunction) or from
problems in the hypothalamus that change
anterior pituitary function (secondary
pituitary dysfunction)
 In either case, one or more hormones may be
undersecreted (pituitary hypofunction) or
oversecreted (pituitary hyperfunction)
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
Pathophysiology
 A person with hypopituitarism has a deficiency of one
or more anterior pituitary hormones, resulting in
metabolic abnormalities and sexual dysfunction

 Decreased production of all of the anterior pituitary
hormones is an extremely rare condition known as
panhypopituitarism

 Deficiencies of adrenocorticotropic hormone (ACTH)
and thyroid-stimulating hormone (TSH) are the most
life threatening because they result in a corresponding
decrease in the secretion of vital hormones from the
adrenal and thyroid glands
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
 Deficiency of the gonadotropins (luteinizing hormone
[LH] and follicle-stimulating hormone [FSH]—hormones
that stimulate the ovaries and testes to produce sex
hormones) changes sexual function in both men and
women

 In males, gonadotropin deficiency results in testicular
failure, with decreased testosterone production from the
Leydig cells and decreased or absent spermatogenesis
from the seminiferous tubules. Decreased testosterone
levels in males cause delayed onset of puberty and
sterility

 In females, gonadotropin deficiency results in ovarian
failure, amenorrhea, and infertility
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
 Growth hormone (GH) deficiency changes tissue
growth patterns indirectly. GH itself has little effect
on tissues and cells. Rather, the presence of GH
stimulates the liver to produce substances known
as somatomedins

 These somatomedins, especially somatomedin С
(insulin-like growth factor-1 [IGF-1]), then enhance
growth activities in cells and tissues. Somatomedin
С is responsible for bone and cartilage growth and
maintenance
DISORDERS OF THE ANTERIOR PITUITARY GLAND.
Hypopituitarism
 GH deficiency may be a result of insufficient
production of GH, failure of the liver to produce
somatomedins, or a failure of the cells or tissues to
respond to the presence of the somatomedins

 GH deficiency in children leads to short stature and
other manifestations of growth retardation

 GH deficiency in adults produces no obvious
anatomic changes but does increase the rate of
bone destructive activity, leading to thinner, more
fragile bones
DISORDERS OF THE ANTERIOR PITUITARY GLAND.
Hypopituitarism
Etiology
 The cause of hypopituitarism varies
 Benign or malignant pituitary tumors can compress
and destroy pituitary tissue.
 Pituitary function can be impaired by severe
malnutrition or rapid loss of body fat, such as in
people with anorexia nervosa (a disorder in which
people see themselves as overweight and eat so little
that excessive weight loss and starvation result)
 Poor circulation to the pituitary gland can cause
hypoxia and infarction
 Idiopathic hypopituitarism may result in an
isolated hormone deficiency, and often the cause is
unknown
DISORDERS OF THE ANTERIOR PITUITARY GLAND.
Hypopituitarism
 Postpartum hemorrhage is the most common cause
of pituitary infarction, which results in decreased
hormone secretion. This clinical problem is known
as Sheehan's syndrome
 The pituitary gland normally enlarges during
pregnancy, and when hypotension results from
hemorrhage, ischemia and necrosis of the gland
occur
 Usually this condition develops immediately
postpartum, although some cases have occurred
several years after delivery
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
Assessment
Anterior Pituitary Hormones
 Growth hormone (GH) Decreased bone density
Pathologic fractures
Decreased muscle strength
Increased serum cholesterol levels

 Gonadotropins Women:
(luteinizing • Amenorrhea
hormone [LH], • Anovulation
folliclestimulating • Low circulating estrogen levels
hormone [FSH]) • Breast atrophy
• Loss of bone density
• Decreased axillary and pubic hair
• Decreased libido
• Fine facial wrinkles
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
Men:
• Decreased facial hair
• Decreased ejaculate volume
• Reduced muscle mass
• Loss of bone density
• Decreased body hair
• Decreased libido
• Impotence
• Fine facial wrinkles
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
 Thyrotropin Decreased circulating TSH levels
(Thyroid-stimulating Decreased circulating thyroid
hormone [TSH]) hormone levels
Weight gain
Intolerance to cold
Scalp alopecia
Hirsuitism
Menstrual abnormalities
Decreased libido
Slowed cognition
Lethargy
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
 Adrenocorticotropic Decreased serum cortisol levels
hormone (ACTH) Pale, sallow complexion
Malaise and lethargy
Anorexia
Postural hypotension
Headache
Hypoglycemia
Hyponatremia
Decreased axillary and pubic
hair (women)
DISORDERS OF THE GLAND.
Hypopituitarism
Posterior Pituitary Hormones
 Vasopressin (antidi- Diabetes insipidus
uretic hormone • Greatly increased
[ADH]) urine output
• Low urine specific gravity
(< 1.005)
• Hypovolemia
Hypotension
Dehydration
• Increased plasma osmolarity
• Increased thirst
• Output does not decrease
when fluid intake decreases
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
 Neurologic manifestations of
hypopituitarism due to tumor growth often
first occur as changes in visual perception
 The nurse evaluates the client's visual
acuity, particularly peripheral vision, for
changes or loss
 Bilateral temporal headaches are a common
finding
 Other manifestations may include diplopia
(double vision) and ocular muscle paralysis,
limiting eye movement
DISORDERS OF THE ANTERIOR PITUITARY GLAND.
Hypopituitarism
Stimulation tests
 The presence of insulin in people with normal pituitary function
causes an increased release of GH and ACTH. The stimulation test
for either GH or ACTH assessment involves injecting the client with
regular insulin (0.05 to 1 units/kg of body weight) and checking
the circulating levels of GH and ACTH

 The stimulation test for TSH involves injecting thyrotropin-
releasing hormone (TRH) and measuring the blood levels of
thyroid hormones

 The stimulation test for LH and FSH involves administering
gonadotropin-releasing hormone (GnRH). In people with no
pituitary problems, this injection results in a peak release of LH
and FSH within 15 to 45 minutes after the injection

 The stimulation test for PRL is the same as that for TSH
DISORDERS OF THE ANTERIOR PITUITARY GLAND.
Hypopituitarism
 Pituitary abnormalities may cause changes
in the sella turcica (the bony nest where
the pituitary gland rests) that can be seen
with skull x-ray studies
 Such changes may include enlargement,
erosion, and calcifications in the area of the sella
turcica as a result of pituitary tumors

 An angiogram may be indicated to rule out
the presence of an aneurysm or congenital
vascular malformations, especially before
any surgical intervention
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
Interventions
 Management of the adult with hypopituitarism focuses on
replacement of deficient hormones
 Men who have gonadotropin deficiency are treated with
androgens (testosterone). The most widely used and most
effective route of administration is intramuscular (IM),
although use of transdermal testosterone patches is
increasing
 Therapy isusually initiated with high-dose testosterone and
is continued until virilization (presence of male secondary
sex characteristics) is achieved. The dose may then be
decreased, but therapy continues throughout life
 Androgen therapy is avoided in men with prostate cancer.
 Side effects of testosterone therapy include gynecomastia
(the development of breast tissue in men), baldness, and
prostatic hypertrophy
DISORDERS OF THE PITUITARY GLAND.
Hypopituitarism
 Women who have gonadotropin deficiency receive
hormone replacement with a combination of estrogen
and progesterone administered at their menstrual
cycle, which causes withdrawal bleeding
 The risk for hypertension or thrombosis (formation
of blood clots in deep veins) is increased with
estrogen therapy, especially among women who
smoke
 For women who wish to become pregnant, clomiphene
citrate (Clomid) may be given to induce ovulation.
Menotropins in conjunction with human chorionic
gonadotropin (hCG) are used to stimulate ovulation
when therapy with clomiphene citrate has failed
DISORDERS OF THE PITUITARY GLAND.
Hyperpituitarism
 Hyperpituitarism is a condition of
hormone oversecretion that occurs when a
client has pituitary tumors or hyperplasias
 PRL-secreting tumors are the most common
of the pituitary adenomas. Excessive PRL
secretion inhibits the secretion of gonadal
steroids and gonadotropins in men and
women, resulting in galactorrhea
(production of breast milk), amenorrhea,
and infertility
DISORDERS OF THE PITUITARY GLAND.
Hyperpituitarism
 Overproduction of GH results in gigantism
or acromegaly
 In the client with gigantism, the onset of
GH hypersecretion occurs before puberty,
which causes rapid proportional growth in
the length of all bones
 In the client with acromegaly, excessive GH
secretion occurs after puberty and produces
increased skeletal thickness, hypertrophy of
the skin, and enlargement of many visceral
organs, such as the liver and heart
DISORDERS OF THE PITUITARY GLAND.
Hyperpituitarism
DISORDERS OF THE PITUITARY GLAND.
Hyperpituitarism
History
 The nurse obtains data about the client's age, gender, and
family history
 The client is asked about any change in hat, glove, ring, or
shoe size
 Fatigue and lethargy are common
 The client with excessively high GH levels may have backache
and arthralgias (joint pain) in response to bone changes
 He or she is asked specifically about the presence of headaches
and changes in vision
 The client with hypersecretion of PRL (hyperprolactinemia)
often reports difficulties in sexual functioning
 The nurse asks women about menstrual changes (e.g.,
amenorrhea, irregular menses, and difficulty in achieving
pregnancy) and about decreased libido or dyspareunia
(painful intercourse)
 Men may report decreased libido and impotence
DISORDERS OF THE PITUITARY GLAND.
Hyperpituitarism
History
 The nurse obtains data about the client's age, gender, and
family history
 The client is asked about any change in hat, glove, ring, or
shoe size
 Fatigue and lethargy are common
 The client with excessively high GH levels may have backache
and arthralgias (joint pain) in response to bone changes
 He or she is asked specifically about the presence of headaches
and changes in vision
 The client with hypersecretion of PRL (hyperprolactinemia)
often reports difficulties in sexual functioning
 The nurse asks women about menstrual changes (e.g.,
amenorrhea, irregular menses, and difficulty in achieving
pregnancy) and about decreased libido or dyspareunia
(painful intercourse)
 Men may report decreased libido and impotence
DISORDERS OF THE PITUITARY GLAND.
Hyperpituitarism
DISORDERS OF THE PITUITARY GLAND.
Hyperpituitarism
Suppression tests
 High circulating levels of glucose have a suppressive
effect on the release of GH. In a suppression test, 100
g of oral glucose or 0.5 g/kg of body weight is given
intravenously. GH levels are measured serially for up
to 120 minutes. GH levels that do not fall below 5
ng/mL indicate a positive (abnormal) result

 Administration of intravenous (IV) cortisol in the form
of dexamethasone (Decadron). This agent should
result in suppression of ACTH. When ACTH production
continues in the presence of dexamethasone
administration, the client may have pituitary
Cushing's disease
DISORDERS OF THE PITUITARY GLAND.
Hyperpituitarism
Interventions
 NONSURGICAL MANAGEMENT
 DRUG THERAPY
 bromocriptine mesylate (Parlodel) 7.5
mg/day - stimulates dopamine receptors in
the brain and inhibits the release of many
pituitary hormones, most specifically GH
and PRL
 RADIATION THERAPY
 SURGICAL MANAGEMENT
DISORDERS OF THE PITUITARY GLAND.
Hyperpituitarism
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
 Disorders of the posterior pituitary
(neurohypophysis) are directly related to
a deficiency or excess of the hormone
vasopressin (antidiuretic hormone
[ADH])
 Two disorders associated with ADH
deficiency or excess are diabetes insipidus
and the syndrome of inappropriate
antidiuretic hormone (SIADH)
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
Diabetes Insipidus
 Diabetes insipidus is a disorder of water metabolism
caused by a deficiency of ADH—either a decrease in
ADH synthesis or an inability of the kidneys to
respond appropriately to ADH
 ADH deficiency results in the excretion of large
volumes of dilute urine. Without the presence of ADH,
the distal tubules and collecting ducts of the kidney
remain impermeable to water. Thus water is excreted
as urine rather than being absorbed in these areas,
which leads to polyuria (excessive urination with loss
of free water)
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
 ADH deficiency can be classified as nephrogenic,
drugrelated, primary, or secondary

 Nephrogenic diabetes insipidus is an inherited
disorder. The renal tubules do not respond to the
actions of ADH, which results in inadequate water
reabsorption by the kidney. The actual amount of
hormone produced is not deficient.

 Primary diabetes insipidus is caused by a defect in the
hypothalamus or pituitary gland, resulting in a lack of
ADH production or release
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
 Secondary diabetes insipidus results from tumors
within or adjacent to the hypothalamus or pituitary
gland, head trauma, infectious processes, surgical
procedures (hypophysectomy), or metastatic tumors,
usually from the lung or the breast. Less commonly, it
is caused by brain hemorrhage, brain disease, or
cerebral aneurysm

 Drug-related diabetes insipidus is caused by the
administration of lithium carbonate (Eskalith, Lithobid,
Carbolith) and demeclocycline (Declomycin). These
drags can interfere with the kidneys' response to ADH
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
Assessment
 Most of the clinical manifestations of diabetes
insipidus are related to dehydration
 The nurse notes the key symptoms of an increase in
the frequency of urination and excessive thirst
 The client is asked about a history of any known
etiologic factors, such as recent surgery, head
trauma, or medication use (e.g., lithium)
 Although increased fluid intake usually prevents
serious dehydration and volume depletion, the client
who is deprived of fluids or who cannot increase oral
fluid intake may experience shock caused by fluid loss
and plasma hyperosmolality
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
 Signs of dehydration, such as
poor skin turgor and dry or
cracked mucous membranes
or skin, may be present in
varying degrees
*Occurs when access to water is
limited and rapid dehydration results
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
 Loss of free water produces expected changes in
blood and urine tests. The initial step in diagnosis is to
measure a 24-hour fluid intake and output. The
amount of the client's food and fluid is not restricted
during this measurement. Urine output must be more
than 4 L during this period for diabetes insipidus to be
diagnosed. The amount of urine excreted in 24 hours
may vary from 4 to 30 L/day. Urine is dilute and
therefore has a low specific gravity (less than 1.005)
and low osmolality (50 to 200 mOsm/kg)

 Fluid deprivation and hypertonic saline tests are also
used for diagnosis of the disorder
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
Interventions
 Medical management is aimed at controlling the
symptoms of the disease through drag therapy.
 If only a partial deficit of ADH is present, effective
control can be achieved with oral chlorpropamide or
clofibrate.
 These drags increase the action of existing ADH and
possibly have a direct stimulating effect on the
production of ADH in the hypothalamus. They have
some undesirable side effects, however, and are not
used as often as synthetic vasopressin
 When ADH deficiency is severe, ADH is replaced in
amounts sufficient to maintain water balance
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
Syndrome of Inappropriate Antidiuretic Hormone
 The syndrome of inappropriate antidiuretic
hormone (SIADH) occurs when vasopressin
(antidiuretic hormone [ADH]) is secreted even when
plasma osmolality is low or normal
 SIADH is also known as the Schwartz-Bartter syndrome

 ADH continues to be released even when plasma is
hyposmolar. Water is retained, which results in dilutional
hyponatremia (a decreased serum sodium level due to
dilution) and expansion of the extracellular fluid volume.
The increase in plasma volume causes an increase in the
glomerular filtration rate and inhibits the release of renin
and aldosterone. The combined effect is an increased
sodium loss in urine, further contributing to
hyponatremia
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
HISTORY
 The nurse pays particular attention to
a history of the following:
 Recent trauma
 Cerebrovascular disease
 Tuberculosis or other pulmonary disease
 Cancer
 All past and current medication use
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
Assessment
 Initially, the symptoms of SIADH are related to water retention.
 Gastrointestinal (GI) disturbances may occur first:
 loss of appetite
 nausea and vomiting
 The nurse weighs the client and documents any recent weight gain

 The client may experience lethargy, headaches, hostility, and
disorientation. A change in level of consciousness is an early sign
of SIADH. Neurologic symptoms can progress from lethargy and
headaches to decreased responsiveness, seizures, and coma.
 The nurse assesses deep tendon reflexes, which are often
decreased or sluggish.
 Vital sign changes include tachycardia (caused by the increased
fluid volume) and hypothermia (caused by central nervous system
disturbance)
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
Diagnostic assessment
 Water retention changes both plasma and urine osmolality.
 Urine volume decreases, and urine osmolarity increases.
 Plasma volume increases, and plasma osmolarity
decreases.
 Elevated urine sodium levels and elevated specific gravity
reflect increased urine concentration.
 Serum sodium levels are decreased, often as low as 110
mEq/L, because of volume expansion and sodium excretion.

 Radioimmunoassay of ADH can diagnose SIADH when ADH
levels are inappropriately elevated in relation to plasma
 osmolality. (When plasma osmolality is normal or ecreased,
ADH levels should be low)
DISORDERS OF THE POSTERIOR
PITUITARY GLAND
Interventions
 Interventions to treat SIADH focus on
restricting fluid intake, promoting the
excretion of water, replacing lost sodium,
interfering with the action of ADH, and
preventing injury if the client experiences
increased cranial pressure or seizures.
 FLUID RESTRICTION (500 to 600 mL/24 hr)
 DRUG THERAPY. Diuretics, Hypertonic
saline (3% sodium chloride [3% NaCl])
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
 Insufficiency of adrenocortical steroids causes problems
through the loss of mineralocorticoid (aldosterone) and
glucocorticoid (cortisol) action

 Impaired secretion of cortisol results in decreased
gluconeogenesis, leading to hypoglycemia. The
glomerular filtration rate and gastric acid production
decrease, leading to a reduction in urea nitrogen excretion,
causing anorexia and weight loss

 Reduced aldosterone secretion causes potassium, sodium,
and water imbalances. Potassium excretion is
decreased,causing hyperkalemia; sodium and water
excretion is increased, causing hyponatremia and
hypovolemia. Potassium retention also promotes
reabsorption of hydrogen ions, which can ultimately lead to
acidosis
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
 Acute adrenal insufficiency, or Addisonian
crisis, is a ifethreatening event in which
the physiologic need for glucocorticoid and
mineralocorticoid hormones is greater than
the available supply

 In most cases, acute adrenal insufficiency
occurs in response to a stressful event
(e.g., surgery, trauma, or severe infection),
especially when the adrenal hormone
output is already compromised
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
HISTORY
 The client is asked about any change in activity level, because
lethargy, fatigue, and muscle weakness are often present
 Questions about salt intake are included because salt craving is
often a symptom of adrenal hypofunction
 Gastrointestinal (GI) problems, such as anorexia, nausea,
vomiting, diarrhea, and abdominal pain, often occur. The nurse
asks about weight loss during the past weeks or months
 Female clients report menstrual changes related to weight loss,
and male clients may report impotence
 The nurse asks whether the client has had radiation
 to the abdomen or head.
 Significant medical problems (e.g., tuberculosis or previous
intracranial surgery) and all past and current medications,
especially steroids, anticoagulants, or cytotoxic drugs, are
documented
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
HISTORY
 The client is asked about any change in activity level, because
lethargy, fatigue, and muscle weakness are often present
 Questions about salt intake are included because salt craving is
often a symptom of adrenal hypofunction
 Gastrointestinal (GI) problems, such as anorexia, nausea,
vomiting, diarrhea, and abdominal pain, often occur. The nurse
asks about weight loss during the past weeks or months
 Female clients report menstrual changes related to weight loss,
and male clients may report impotence
 The nurse asks whether the client has had radiation
 to the abdomen or head.
 Significant medical problems (e.g., tuberculosis or previous
intracranial surgery) and all past and current medications,
especially steroids, anticoagulants, or cytotoxic drugs, are
documented
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS

 The clinical manifestations of adrenal hypofunction vary,
and the severity of symptoms is related to the degree of
hormone deficiency
 In clients with primary adrenal hypofunction, plasma ACTH
and melanocyte-stimulating hormone (MSH) levels are
elevated because of the loss of the adrenal-hypothalamic-
pituitary feedback system. Elevated MSH levels result in
areas of increased pigmentation
 In primary autoimmune disease, areas of decreased
pigmentation may occur because of destruction of
pigmentproducing cells in the skin (melanocytes). Body hair
may also be decreased
 In secondary disease, there is no increase in skin
pigmentation
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
 The nurse assesses the client for symptoms
of hypoglycemia (e.g., sweating,
headaches, tachycardia, and tremors) and
volume depletion (postural hypotension and
dehydration)
 Hyperkalemia (elevated blood levels of
potassium) can cause dysrhythmias with an
irregular heart rate and result in cardiac
arrest
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
PSYCHOSOCIAL ASSESSMENT
 Depending on the degree of metabolic
imbalance, clients may appear lethargic,
apathetic, depressed, confused, and even
psychotic. The nurse observes the client
and checks his or her orientation to person,
place, and time. Families may report that
the client has a decreased energy level,
experiences wide mood swings, and is
forgetful
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
 Plasma cortisol levels fail to rise during stimulation
tests
 Urinary 17-hydroxycorticosteroids are the
glucocorticoid metabolites, and 17-ketosteroid levels
reflect the adrenal androgen metabolites. Both levels
are in the low or low-normal range in adrenal
hypofunction
 Skull x-ray films, computed tomography (CT),
magnetic resonance imaging (MRI), and arteriography
may aid in the search for a cause of pituitary
problems leading to adrenal insufficiency
 Noninvasive procedures of the adrenal gland, such as
CT scans without dye, may occasionally show atrophy
of the gland. CT scans may help determine adrenal
hypofunction
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
 A rapid ACTH stimulation test may be administered on an
outpatient basis. Cosyntropin 0.25 to 1 mg is given
intramuscularly or intravenously, and plasma cortisol levels
are obtained at 30-minute and 1-hour intervals after the
baseline value is established. In primary insufficiency, the
cortisol response is absent or markedly decreased; in
secondary insufficiency, it is decreased

 A longer ACTH stimulation test uses a continuous infusion of
50 units of ACTH in saline for 24 hours or an 8-hour
infusion daily for 4 to 5 days, with simultaneously collected
24-hour urine samples. Levels of urinary 17-
hydroxycorticosteroids and urinary free cortisol are also
measured. In clients with primary adrenal insufficiency, the
response is low or absent; in those with secondary
insufficiency, the value for 17-hydroxycorticosteroids fails
to rise above 20 mg per total volume
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
Interventions
 Nursing interventions are aimed at
promoting fluid balance and monitoring for
fluid deficit
 The nurse or assistive nursing personnel
weighs the client daily and records intake
and output. Vital signs are assessed every
1 to 4 hours, depending on the client's
condition and the occurrence of
dysrhythmias or postural hypotension.
Laboratory values are monitored to identify
hemoconcentrations
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPOFUNCTION
 Glucocorticoid and mineralocorticoid deficiencies are
completely corrected by replacement therapy.
Hydrocortisone corrects glucocorticoid deficiency

 An additional mineralocorticoid hormone, such as
fludrocortisone (Florinef), may be needed to maintain
correct electrolyte balance (especially sodium and
potassium). Adjustments in dosage may be necessary
in hot weather, when additional sodium is lost
because of excessive perspiration

 Salt restriction or diuretic therapy should not be
started without considering whether it might
precipitate an adrenal crisis
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Hypersecretion by the adrenal cortex may result in
excessive amounts of glucocorticoids, leading to
hypercortisolism (e.g., Cushing's syndrome),
hyperaldosteronism (excessive mineralocorticoid
production), or excessive androgen production

 Hypersecretion of the adrenal medulla caused by a
tumor (pheochromocytoma) results in excessive
secretion of catecholamines, of which 80% is
epinephrine and the remainder is norepinephrine
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
Hypercortisolism (Cushing's Syndrome)
 Excessive stimulation of adrenocorticotropic
hormone (ACTH) of either pituitary or
ectopic origin causes adrenocortical
hyperplasia, which results in loss of normal
hormone secretion rhythms

 The client's endocrine tissues have
decreased responsiveness to releasing
hormones, especially prolactin (PRL),
thyrotropin, and gonadotropin. Many clients
also experience abnormal sleep patterns
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 The client with Cushing's syndrome has alterations of
nitrogen, carbohydrate, and mineral metabolism. An
increase in total body fat results from slow turnover of
plasma fatty acids, and a redistribution of fat
produces the typical body pattern of trancal obesity,
"buffalo hump," and "moon face“
 Increases in the breakdown of tissue protein and an
increase in urine nitrogen excretion also occur,
resulting in decreased muscle mass, atrophic (thin)
skin, and bone density loss
 High levels of corticosteroids kill lymphocytes and
shrink organs containing lymphocytes, such as the
liver, the spleen, and the lymph nodes. Thus
protection of the inflammatory and immune responses
is reduced
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 In most cases, increased androgen
production causes acne, hirsutism
(increased hair growth), and occasionally,
clitoral hypertrophy
 Increased androgen production can also
interrupt the normal hormone feedback
mechanism for the ovary, decreasing the
ovary's production of estrogens and
progesterone. Oligomenorrhea (scant or
infrequent menses) occurs as a result
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
Etiology
 Cushing's syndrome is a group of clinical problems
caused by an excess of cortisol, secreted by the
adrenal cortex (endogenous) or administered for
another clinical disorder (exogenous or iatrogenic).
Women are affected eight times more often than men
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
HISTORY
 The nurse asks about changes in activity or sleep
patterns, fatigue, and muscle weakness. Osteoporosis
is common in hypercortisolism, and the client is asked
about bone pain or a history of fractures. The nurse
also questions the client about a history of frequent
infections and easy bruising, which suggest
hypercortisolism. Women may report a cessation of
menses
 Gastrointestinal (GI) complaints may indicate ulcer
formation from increased hydrochloric acid secretion
 The nurse also refers to the client's medical history.
Steroid or alcohol abuse can produce the clinical and
biochemical features of Cushing's syndrome
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS
 The client with hypercortisolism has characteristic physical
changes. The general appearance of the client is observed.
Changes in fat distribution may result in fat pads on the
neck, back, and shoulders ("buffalo hump"); an enlarged
trunk with thin arms and legs; and a round face ("moon
face"). Other characteristics include generalized muscle
wasting and weakness

 The nurse also inspects the client for skin changes resulting
from increased blood vessel fragility, such as bruises, thin
or translucent skin, and wounds that have not healed
properly

 Reddish purple striae ("stretch marks") are often present
on the abdomen, upper thighs, and upper arms because of
the degradative effect of cortisol on collagen
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Excessive cortisol secretion may result in a
fine coating of hair over the face and body
and in acne. In the female client, the nurse
looks for the presence of hirsutism, clitoral
hypertrophy, and male pattern balding
related to androgen excess
 Elevations in blood glucose levels are also a
frequent finding
 Hypertension from water and sodium
retention is common
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
PSYCHOSOCIAL ASSESSMENT
 Hypercortisolism can result in
emotional lability, and the nurse asks
about mood swings, irritability,
confusion, or depression

 The client may become neurotic or
psychotic as a result of changes in
blood cortisol levels
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
DIAGNOSTIC ASSESSMENT
 Plasma cortisol levels are elevated in clients with
hypercortisolism.
 Blood for cortisol assays is obtained at the same time
of day because levels vary throughout the day.
 Plasma ACTH levels vary, depending on the cause of
hypercortisolism
 In ectopic (ACTHproducing) syndromes, ACTH levels
are elevated.
 In Cushing's syndrome (primary disease of the
adrenal gland), ACTH levels are low to immeasurable
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Additional laboratory findings may
include the following:
 Increased blood glucose level
 Elevated white blood cell count
 Elevated lymphocyte count
 Increased sodium level
 Decreased serum calcium level
 Decreased serum potassium level
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Urine is tested to measure levels of free cortisol
and the adrenal metabolites of cortisol and
androgens (17-hydroxycorticosteroids and 17-
ketosteroids)

 The client is instructed to save all urine for 24
hours

 In Cushing's disease, basal levels of urinary free
cortisol, 17-ketosteroids, and 17-
hydroxycorticosteroids are all elevated, as are urine
levels of calcium, potassium, and glucose
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Radiographic studies, computed
tomography (CT) scans, magnetic
resonance imaging (MRI), and
arteriography may identify lesions of
the adrenal or pituitary glands, lung,
GI tract, or pancreas in a client with
clinical manifestations of cortisol
hypersecretion
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 The overnight dexamethasone
suppression test is an initial screening
test for Cushing's syndrome. The client is
instructed not to take medications,
especially phenytoin (Dilantin) or
phenobarbital, for at least 2 days before
the test. Normally, plasma cortisol levels
are lower than 5 (xg/dL). Higher levels
indicate that further, definitive testing is
necessary
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 For the 3-day, low-dose dexamethasone suppression test,
the client must take no medications for at least 2 days
before the test (if possible) and have no stressful
procedures (e.g., barium enema, myelogram, or an intense
physical therapy session) performed during the test
 A baseline 24-hour urine sample is collected on day 1.
Dexamethasone 0.5 mg is administered every 6 hours on
days 2 and 3, during which time 24-hour urine collections
are taken
 The 24-hour urine collections are tested for 17-
ketosteroids, 17-hydroxycorticosteroids, creatinine, and
urinary free cortisol
 Normally, urinary 17-hydroxycorticosteroid excretion and
free cortisol levels are suppressed by dexamethasone, and
Cushing's syndrome is ruled out. If these levels are not
suppressed, a higher-dose dexamethasone test is
performed
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 The high-dose (8-mg) dexamethasone suppression
test distinguishes between bilateral adrenocortical
hyperplasia (e.g., Cushing's syndrome) and an
adrenocortical neoplasm as the cause of
hypercortisolism

 This test can be performed as an overnight test or a
2-day test and is similar to the tests previously
discussed but uses higher doses of dexamethasone

 In the overnight high-dose test, the client with
Cushing's disease will have a reduced plasma cortisol
level that is less than 50% of baseline. This test is
more reliable than the 2-day high-dose test
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
Interventions
 Goals of treatment for hypercortisolism include
reduction of plasma cortisol levels, removal of
tumors, prevention of complications, and
restoration of normal or acceptable body
appearance

 Preoperative and postoperative nursing care is an
integral part of the management of the client with
endogenous hypercortisolism because surgical
intervention is usually necessary for the relief of
symptoms
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
NONSURGICAL MANAGEMENT. The nurse weighs the
client daily and monitors intake and output to assess
hydration status. Restriction of fluid intake is
sometimes necessary to maintain fluid balance

 DRUG THERAPY. Most clients with endogenous
hypercortisolism undergo surgery. Drugs that
interfere with adrenocorticotropic hormone (ACTH)
production or adrenal hormone synthesis, however,
may be used for palliation.
 Mitotane (Lysodren) is an adrenal cytotoxic agent
used for inoperable adrenal tumors
 Aminoglutethimide (Elipten, Cytadren) is an adrenal
enzyme inhibitor that decreases cortisol production
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Trilostane (Modrastane), also an enzyme
inhibitor, has not always been effective
 Cyproheptadine (Periactin) is less commonly
used to treat clients with adrenal hyperfunction
resulting from pituitary-related Cushing's
disease because it interferes with ACTH
production
 During all drug therapy, the nurse assesses
the client for therapy effectiveness and side
effects or symptoms of toxicity
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
RADIATION THERAPY. Radiation, applied internally or
externally, may be used to treat hypercortisolism
caused by pituitary adenomas. However, radiation is
not always effective and also may destroy normal
tissue
 The nurse observes for any changes in the client's
neurologic status, such as headache, elevated blood
pressure or pulse, disorientation, or changes in pupil
size or reaction
 The client may experience skin dryness, redness,
flushing, or alopecia at the radiation site
 The nurse reviews these possible side effects with the
client
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
SURGICAL MANAGEMENT. The surgical treatment of
adrenocortical hypersecretion depends on the cause
of the disease
 When adrenal hyperfunction is due to increased
pituitary secretion of ACTH, transsphenoidal removal
of an adenoma may be attempted. In many instances,
small adenomas cannot be localized and
hypophysectomy is needed. Hypophysectomy is
performed via the transsphenoidal or transfrontal
craniotomy route
 If hypercortisolism is caused by adrenal adenomas or
carcinomas, a partial or complete adrenalectomy
(removal of the adrenal gland) may be needed
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 PREOPERATIVE CARE. Electrolyte imbalances are
corrected before surgery, and the nurse monitors
potassium, sodium, and chloride values.
Dysrhythmias from potassium imbalance may occur,
and cardiac monitoring may be indicated.

 Hyperglycemia, if present, is controlled before
surgery, and the nurse monitors blood glucose levels.

 The nurse and assistive nursing personnel attempt to
prevent infection with handwashing and aseptic
technique.
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 The risk for falls is decreased by raising the siderails
of the bed and encouraging the client to ask for
assistance when getting out of bed.

 Glucocorticoid preparations are administered
preoperatively as ordered. The client continues to
receive glucocorticoids throughout the operative
procedure to prevent adrenal crisis. The removal of
the tumor results in a sudden drop in cortisol levels.

 The nurse discusses postoperative care and long-term
medication therapy during preoperative teaching
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 OPERATIVE PROCEDURES. A unilateral
adrenalectomy is performed when one gland is
involved. A bilateral adrenalectomy is necessary
when ectopic ACTH-producing tumors cannot be
treated by other means or when both adrenal glands
are diseased

 Surgery can be abdominal or through the lateral
flank. Abdominal surgery causes a higher degree of
illness and risk. In the flank approach (the preferred
approach), the abdominal cavity is not entered, and
the morbidity and mortality rates are reduced. A new
approach, laparoscopic adrenalectomy, may reduce
the incidence of some postoperative complications
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 POSTOPERATIVE CARE. After an adrenalectomy, the client is
usually sent to a critical care unit.
 In the immediate postoperative period, the nurse assesses the
client every 15 minutes to identify symptoms of cardiovascular
collapse or shock (e.g., hypotension, a rapid, weak pulse, and
a decreasing urine output) due to possible insufficient
glucocorticoid replacement.
 The nurse monitors ongoing vital signs and other
hemodynamic variables (central venous pressure, pulmonary
wedge pressure), intake and output, daily weights, and serum
electrolyte levels.
 After a bilateral adrenalectomy, clients require lifelong
glucocorticoid and mineralocorticoid replacement. The nurse
administers glucocorticoid preparations as ordered.
 In unilateral adrenalectomy, glucocorticoid replacement
continues until the remaining gland increases hormone
production. This therapy may be required for up to 2 years
after surgery
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 PREVENTING COMPLICATIONS.
The client who has hypercortisolism is
prone to injury from skin breakdown,
pathologic bone fractures, and
gastrointestinal (GI) bleeding.

 Prevention of such injuries is a major
nursing care focus
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Gastrointestinal Bleeding. Interventions are
aimed at minimizing gastric irritation,
usually through drug therapy

 Drug therapy involves two different types
of agents: those that protect the GI mucosa
(antacids) and those that decrease the
secretion of hydrochloric acid (H
2
-blockers,
inhibitors of gastric proton pump)
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
Hyperaldosteronism
 In clients with hyperaldosteronism, increased
secretion of aldosterone results in mineralocorticoid
excess.
 Primary hyperaldosteronism (Conn's syndrome) is due
to excessive secretion of aldosterone from one or both
adrenal glands, which is most commonly caused by an
adenoma.
 In a person with secondary hyperaldosteronism, the
continuous excessive secretion of aldosterone is
caused by high levels of angiotensin II that are due to
high plasma renin activity. Causes of this renin
activation include renal hypoxemia and the use of
thiazide diuretics.
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Increased aldosterone levels affect the renal tubules and
cause sodium retention with potassium and hydrogen ion
excretion.

 Hypernatremia, hypokalemia, and metabolic alkalosis
result.

 Sodium retention increases blood and interstitial fluid
volume, which elevates blood pressure and suppresses
renin production. The elevated blood pressure may cause
strokes and renal damage.

 Peripheral edema rarely occurs because of the "renal
escape mechanism," in which the proximal tubule decreases
sodium reabsorption. However, no compensatory
mechanism exists to stop or reverse the loss of potassium
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
Assessment
 Symptoms related to hypokalemia and elevated blood
pressure are the most common problems of the client
with hyperaldosteronism.
 The history may reveal nonspecific findings, such as
headache, fatigue, muscle weakness, nocturia
(excessive urination at night), and loss of stamina.
 Polydipsia (excessive fluid intake) and polyuria
(excessive urine output) occur less frequently.
 Paresthesias (sensations of numbness and tingling)
may occur if potassium depletion is severe. The client
may have visual changes related to hypertension
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 The diagnosis of primary hyperaldosteronism is made
on the basis of laboratory studies and x-ray findings.
 Serum potassium levels are decreased, and sodium
levels are elevated.
 Plasma renin levels are low; aldosterone levels are
elevated.
 Increased hydrogen ion secretion results in metabolic
alkalemia (elevated blood pH).
 Urine studies show low specific gravity and elevated
aldosterone levels.
 Computed tomography (CT) scans reveal the
presence and location of adrenal adenomas
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
Interventions
 Surgery is the treatment of choice for
hyperaldosteronism if the problem is identified in its
early stages.

 Adrenalectomy may be unilateral or bilateral. Surgery
is not performed, however, until the client's
potassium levels are normal.

 The physician orders spironolactone (Aldactone,
Novospiroton, Sincomen), a potassium-sparing
diuretic and aldosterone antagonist, to promote fluid
balance. Potassium supplements may be ordered to
increase potassium levels before surgery.
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 The client may also benefit from a low-sodium
preoperative diet, but no dietary restrictions are
needed after surgery because aldosterone levels
should return to normal.

 The client who has undergone a unilateral
adrenalectomy may require temporary glucocorticoid
replacement, and the client who has undergone a
bilateral adrenalectomy needs lifelong replacement.
Glucocorticoids are administered before surgery to
prevent adrenal hypofunction. The client receiving
long-term replacement therapy should wear a medical
alert bracelet
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 When surgery is inadvisable, spironolactone
therapy is continued to control the symptoms
of hypokalemia and hypertension.

 Because spironolactone is a potassium-sparing
diuretic, hyperkalemia can occur in clients who
have impaired renal function or excessive
potassium intake.

 The nurse advises the client to avoid potassium
supplements and foods rich in potassium.
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Because hyponatremia can occur with
spironolactone therapy, the client may require
increased dietary sodium. He or she is instructed to
report symptoms of hyponatremia, such as dryness
of the mouth, thirst, lethargy, or drowsiness.

 The nurse alerts clients to report any additional side
effects of spironolactone therapy, including
gynecomastia, diarrhea, drowsiness, headache,
rash, urticaria (hives), confusion, inability to
maintain an erection, hirsutism, and amenorrhea
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
Pheochromocytoma
 Pheochromocytoma is a catecholamine-
producing tumor that arises in chromaffin
cells
 Pheochromocytomas release the
catecholamines epinephrine and
norepinephrine (NE). Excessive epinephrine
and NE stimulate alpha receptors and beta
receptors and can have wide-ranging
adverse effects mimicking stimulation of
the sympathetic division of the autonomic
nervous system
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
Assessment
 The history may include intermittent hypertensive
episodes or attacks that vary in length from a few
minutes to several hours.
 During these episodes, the client experiences severe
headaches, palpitations, profuse diaphoresis, flushing,
apprehension, or a feeling of impending doom. Pain in
the chest or abdomen, with nausea and vomiting, can
also occur.
 Certain stimuli, such as increased abdominal
pressure, urination, and vigorous abdominal
palpation, can provoke a hypertensive crisis.
 The client may also report heat intolerance, weight
loss, and tremors.
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Diagnostic tests include 24-hour urine collections for
vanillylmandelic acid (VMA) (a product of
catecholamine metabolism), metanephrine, and free
catecholamines, all of which are elevated in the
presence of a pheochromocytoma.
 Basal plasma catecholamine levels are elevated after
the client has been at rest for at least 30 minutes.
 The clonidine suppression test is used in the diagnosis
of a pheochromocytoma. When oral clonidine
hydrochloride (Catapres, Dixarit) is given to a person
who does not have a pheochromocytoma, the
clonidine suppresses catecholamine release and
reduces the serum catecholamine levels. The
response is not seen in the client who has a
pheochromocytoma.
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 When the client suspected of having a
pheochromocytoma has severe hypertension, testing
for the disorder may include alpha-adrenergic
blockade with phentolamine.

 Phentolamine (Regitine, Rogitine) is administered
intravenously at a dose of 5 mg, and blood pressure is
measured every 30 seconds for 3 minutes, then every
minute for 7 minutes.

 When a rapid drop of at least 35 mm Hg systolic
pressure and 25 mm Hg diastolic pressure results, the
test is considered positive
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 After diagnosis, computed
tomography (CT) scans of the adrenal
glands locate intra-adrenal tumors.

 Chest x-ray films and tomograms can
locate tumors in the thoracic area;
arteriograms can locate intra-
abdominal tumors
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
Interventions
 Surgery is the treatment of choice for a
pheochromocytoma. One or both adrenal glands are
removed (depending on whether the tumor is bilateral).
 Preoperatively, the nurse focuses on adequate tissue
perfusion, nutritional needs, and comfort measures.
 The nurse monitors the blood pressure regularly and
places the cuff consistently on the same arm, with the
client in lying and standing positions.
 The nurse also identifies stressors that may precede a
hypertensive crisis and attempts to minimize them. The
client is instructed not to smoke, drink caffeine-
containing beverages, or change position suddenly.
 The abdomen should not be palpated. A diet rich in
calories, vitamins, and minerals is provided.
DISORDERS OF THE ADRENAL GLAND
ADRENAL GLAND HYPERFUNCTION
 Postoperative nursing care is similar to that for the
client who has undergone an adrenalectomy
 The nurse closely monitors the client for hypotension
related to the sudden decrease in catecholamine level
and for hypovolemia, especially when the client was
inadequately prepared for surgery.
 Hemorrhage and shock are possible, and the nurse
administers plasma expanders and fluids as
prescribed.
 Vital signs, as well as fluid intake and output, are
monitored. If opioids are administered, the nurse
observes their effect on blood pressure