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Slide 1
Interventions for Clients with Pituitary and Adrenal Gland
Problems
Slide 2
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
Slide 3
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)
Slide 4
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)
Slide 5
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
Slide 6
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
Slide 7
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
(insulin-like growth factor-1 [IGF-1]), then enhance growth
activities in cells and tissues. Somatomedin is responsible for
bone and cartilage growth and maintenance
Slide 8
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
Slide 9
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
Slide 10
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
Slide 11
DISORDERS OF THE PITUITARY GLAND. Hypopituitarism
Slide 12
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
Slide 13
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
Slide 14
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
Slide 15
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)
Slide 16
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
Slide 17
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
Slide 18
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
Slide 19
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
Slide 20
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
Slide 21
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
Slide 22
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
Slide 23
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
Slide 24
DISORDERS OF THE PITUITARY GLAND. Hyperpituitarism
Slide 25
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
Slide 26
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
Slide 27
Slide 28
DISORDERS OF THE PITUITARY GLAND. Hyperpituitarism
Slide 29
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
Slide 30
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
Slide 31
DISORDERS OF THE PITUITARY GLAND. Hyperpituitarism
Slide 32
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)
Slide 33
DISORDERS OF THE POSTERIOR PITUITARY GLAND Diabetes Insipidus
Diabetes insipidus is a disorder of water metabolism caused by a
deficiency of ADHeither 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)
Slide 34
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
Slide 35
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
Slide 36
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
Slide 37
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
Slide 38
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
Slide 39
DISORDERS OF THE POSTERIOR PITUITARY GLAND
Slide 40
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
Slide 41
DISORDERS OF THE POSTERIOR PITUITARY GLAND
Slide 42
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
Slide 43
DISORDERS OF THE POSTERIOR PITUITARY GLAND
Slide 44
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
Slide 45
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)
Slide 46
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)
Slide 47
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])
Slide 48
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
Slide 49
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
Slide 50
DISORDERS OF THE ADRENAL GLAND ADRENAL GLAND HYPOFUNCTION
Slide 51
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
Slide 52
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
Slide 53
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
Slide 54
DISORDERS OF THE ADRENAL GLAND ADRENAL GLAND HYPOFUNCTION
Slide 55
Slide 56
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
Slide 57
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
Slide 58
DISORDERS OF THE ADRENAL GLAND ADRENAL GLAND HYPOFUNCTION
Slide 59
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
Slide 60
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
Slide 61
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
Slide 62
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
Slide 63
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
Slide 64
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
Slide 65
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
Slide 66
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
Slide 67
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
Slide 68
DISORDERS OF THE ADRENAL GLAND ADRENAL GLAND HYPERFUNCTION
Slide 69
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
Slide 70
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
Slide 71
DISORDERS OF THE ADRENAL GLAND ADRENAL GLAND HYPERFUNCTION
Slide 72
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
Slide 73
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
Slide 74
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
Slide 75
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
Slide 76
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
Slide 77
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
Slide 78
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
Slide 79
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
Slide 80
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
Slide 81
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
Slide 82
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
Slide 83
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
Slide 84
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
Slide 85
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
Slide 86
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.
Slide 87
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
Slide 88
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
Slide 89
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
Slide 90
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
Slide 91
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)
Slide 92
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.
Slide 93
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
Slide 94
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
Slide 95
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
Slide 96
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.
Slide 97
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
Slide 98
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.
Slide 99
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
Slide 100
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
Slide 101
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.
Slide 102
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.
Slide 103
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
Slide 104
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
Slide 105
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.
Slide 106
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