Lewis: Medical-Surgical Nursing, 9th Edition

Chapter 50

Nursing Management: Endocrine Problems

KEY POINTS

ANTERIOR PITUITARY GLAND DISORDER

Acromegaly
Acromegaly is a rare condition resulting from excess
secretion of growth hormone (GH).
In adults, bones increase in thickness and width but not
length.
Manifestations include enlargement of hands and feet,
thickening and enlargement of face and head bony and soft
tissue, sleep apnea, diabetes mellitus, heart failure, and
hypertension.
Treatment focuses on returning GH levels to normal
through surgery, radiation, and drug therapy. Prognosis is
dependent on the age at onset, when treatment is initiated,
and tumor size.
Nursing care for the patient following transsphenoidal
hypophysectomy includes avoidance of vigorous coughing,
sneezing, and straining at stool; elevating the head of bed to
a 30-degree angle at all times; and monitoring neurologic
status. Mild analgesia is used for headaches. Teeth-brushing
is avoided for at least 10 days.
If hypophysectomy is done or pituitary is damaged,
antidiuretic hormone (ADH), cortisol, and thyroid hormone
replacement are needed for life. Patient teaching is essential
with hormone therapy.
HYPOFUNCTION OF PITUITARY GLAND
Hypopituitarism
Hypopituitarism is rare and involves a decrease in
one or more of the tropic hormones, the pituitary hormones
 that are sent as messengers to endocrine glands.
Most deficiencies with hypopituitarism are due to a
pituitary tumor, most often an adenoma.
Signs and symptoms vary with the type and degree of
pituitary dysfunction. Manifestations are related to
hyposecretion of tropic hormones to the target glands.
Treatment consists of surgery or radiation for tumor
removal, followed by lifelong hormone therapy.
DISORDERS OF POSTERIOR PITUITARY GLAND
Syndrome of Inappropriate Antidiuretic Hormone
Syndrome of inappropriate antidiuretic hormone
(SIADH) results from abnormal production or sustained
secretion of ADH. The most common cause is a hormone-
secreting tumor, such as lung cancer.
SIADH is characterized by fluid retention, serum
hypoosmolality, dilutional hyponatremia, hypochloremia,
concentrated urine in presence of normal or increased
intravascular volume, and normal renal function.
Treatment is directed at the underlying cause with a
goal to restore normal fluid volume and osmolality. Fluid
restriction results in gradual, daily weight reductions,
progressive rise in serum sodium concentration and
osmolality, and symptomatic improvement. With chronic
SIADH, patients must learn self-management.
Diabetes Insipidus
Diabetes insipidus (DI) is associated with a
deficiency of production or secretion of ADH or decreased
renal response to ADH. Depending on cause, DI may be
transient or a chronic lifelong condition.
There are three types of DI: central (neurogenic), which
is most common, nephrogenic, and primary.
DI is characterized by polydipsia and polyuria. If oral
fluid intake cannot keep up with urinary losses, severe fluid
volume deficit results as manifested by poor tissue turgor,
hypotension, and hypovolemic shock. The increased urinary
output and plasma osmolality can cause severe fluid and
electrolyte imbalances.
DI is characterized by a dilute urine with urine output at
 greater than 200 mL per hour and specific gravity of less
than 1.005. Identification of cause as central neurogenic DI
often requires a water deprivation test.
For central DI, fluid and hormone therapy is the
cornerstone of treatment.
Nursing care includes early detection, maintenance of
adequate hydration, and patient teaching for long-term
management.
DISORDERS OF THYROID GLAND
Goiter
A goiter is an enlarged thyroid gland.
In a person with a goiter the thyroid cells are stimulated
to grow (process of hyperplasia), which may result in an
overactive thyroid (hyperthyroidism) or an underactive gland
(hypothyroidism).
Thyroid-stimulating hormone (TSH) and T4 levels are
measured to determine the level of thyroid function
associated with the goiter.
Treatment may involve therapy with thyroid hormone to
prevent further thyroid enlargement or surgery to remove
large goiters.
Thyroiditis
Thyroiditis is an inflammatory process in the thyroid
gland.
Subacute and acute forms of thyroiditis have an abrupt
onset with fever, tenderness, and enlargement of the thyroid
gland.
Hashimotos thyroiditis (chronic autoimmune
thyroiditis) is the most common cause of hypothyroidism. A
goiter is present in Hashimotos thyroiditis.
Diagnostic test results and treatment depend on the
type of thyroiditis.
Hyperthyroidism
Hyperthyroidism is hyperactivity of the thyroid gland
with sustained increase in synthesis and release of thyroid
hormones.
Thyrotoxicosis refers to physiologic effects or clinical
syndrome of hypermetabolism resulting from excess
 circulating levels of T4, T3, or both.
Most cases of hyperthyroidism are the result of Graves
disease.
The clinical manifestations of hyperthyroidism are
related to the effect of excess thyroid hormone. Excess
circulating hormone directly increases metabolism and
increases tissue sensitivity to stimulation by the sympathetic
nervous system. When the thyroid gland is large, a goiter
may be noted, and auscultation of thyroid gland may reveal
bruits. A classic finding is exophthalmos, protrusion of
eyeballs from the orbits.
The two primary laboratory findings used to confirm the
diagnosis of hyperthyroidism are decreased TSH levels and
elevated free thyroxine (free T4) levels.
The primary treatment options are antithyroid
medications, radioactive iodine therapy, and subtotal
thyroidectomy.
The overall goals are that the patient with
hyperthyroidism will experience relief of symptoms, have no
serious complications related to the disease or treatment,
maintain nutritional balance, and cooperate with the
therapeutic plan.
Thyrotoxic Crisis
Thyrotoxic crisis, or thyroid storm, is an acute, rare
condition in which all hyperthyroid manifestations are
heightened. Although it can be a life-threatening emergency,
death is rare when treatment is vigorous and initiated early.
Manifestations include severe tachycardia, shock,
hyperthermia, seizures, abdominal pain, diarrhea, delirium,
and coma.
Treatment focuses on reducing circulating thyroid
hormone levels by drug therapy.
Hypothyroidism
Hypothyroidism is a deficiency of thyroid hormone that
causes a general slowing of the metabolic rate.
It may be primary (related to destruction of thyroid
tissue or defective hormone synthesis) or secondary (related
to pituitary disease with decreased TSH secretion or
 hypothalamic dysfunction with decreased thyrotropin-
releasing hormone secretion).
Iodine deficiency is the most common cause worldwide.
When iodine intake is adequate, common causes include
thyroid gland atrophy, related Hashimotos thyroiditis and
Graves disease, and discontinuance of thyroid hormone
therapy.
Hypothyroidism has systemic effects characterized by a
slowing of body processes. Manifestations include fatigue,
lethargy, personality and mental changes, decreased cardiac
output, anemia, and constipation.
Patients with severe long-standing hypothyroidism may
display myxedema, an accumulation of hydrophilic
mucopolysaccharides in dermis and other tissues. This
mucinous edema causes characteristic facies of
hypothyroidism (i.e., puffiness, periorbital edema, and
masklike affect).
A myxedema coma can be precipitated by infection,
drugs (especially opioids, tranquilizers, and barbiturates),
exposure to cold, and trauma. Myxedema coma is
characterized by subnormal temperature, hypotension, and
hypoventilation. To survive, vital functions are supported and
IV thyroid hormone therapy is administered.
Overall treatment in hypothyroidism is restoration of
euthyroid state as safely and rapidly as possible with
hormone replacement therapy. Levothyroxine (Synthroid) is
the drug of choice.
Patient teaching is imperative and need for lifelong
hormone therapy is stressed.
Thyroid Nodules and Cancer
A palpable deformity of the thyroid gland may be
benign or malignant.
Benign nodules are usually not dangerous but can
cause tracheal compression if they become too large.
Thyroid cancer is the most common endocrine-related
cancer.
A major sign of thyroid cancer is the presence of a hard,
painless nodule or nodules on enlarged thyroid gland.
 A thyroidectomy is usually recommended for thyroid
cancer. Surgical procedures may range from unilateral total
lobectomy to near-total thyroidectomy with bilateral
lobectomy. Radioactive iodine therapy and external beam
radiation may be given after surgery.
Nursing care for thyroid cancer is similar to care for
patients who undergo thyroidectomy.
Multiple Endocrine Neoplasia
Multiple endocrine neoplasia is an inherited condition
characterized by presence of hormone-secreting tumors.
The two major types include type 1, mainly
characterized by hyperparathyroidism, and type 2 with
manifestations of medullary thyroid carcinoma. Those with
type 2 may also develop pheochromocytoma.
Treatment includes conservative management
approach (watchful waiting), medications to block excess
hormones, and surgery.
DISORDERS OF PARATHYROID GLANDS
Hyperparathyroidism
Hyperparathyroidism involves increased secretion of
parathyroid hormone (PTH) that leads to hypercalcemia and
hypophosphatemia.
Clinical manifestations include muscle weakness, loss of
appetite, constipation, emotional disorders, and shortened
attention span. Major signs include osteoporosis, fractures,
and kidney stones.
The most effective treatment is a parathyroidectomy.
Nonsurgical treatment involves the avoidance of
immobility, a high fluid intake, and moderate calcium intake.
Drug therapy with agents that lower calcium levels, such as
bisphosphonates, estrogen, oral phosphates, diuretics, and
calcimimetics, may be helpful.
Hypoparathyroidism
Hypoparathyroidism results from inadequate
circulating PTH resulting in hypocalcemia.
The most common cause is iatrogenic from accidental
removal of parathyroid glands or damage to these glands
during neck surgery (usually thyroidectomy).
 Sudden decreases in serum calcium cause tetany,
which is tingling of lips, fingertips, and increased muscle
tension with paresthesias and stiffness. A positive Chvosteks
sign and Trousseaus sign are usually present.
Focus is to treat tetany, maintain normal serum calcium
levels, and prevent long-term complications. Emergency
treatment of tetany requires IV calcium.
The patient requires instruction about lifelong
treatment, including drug therapy, nutrition, and monitoring
of calcium levels.
DISORDERS OF ADRENAL CORTEX
Cushing Syndrome
Cushing syndrome is a clinical condition that results
from chronic exposure to excess corticosteroids, particularly
glucocorticoids.
The most common cause is the administration of
exogenous corticosteroids (e.g., prednisone). Most cases of
endogenous Cushing syndrome are due to an
adrenocorticotropic hormone (ACTH) secreting pituitary
tumor (pituitary adenoma or adrenal tumor).
Key manifestations include central or generalized
obesity, moon facies (fullness of face), purplish-red striae
below the skin surface, hirsutism in women, hypertension,
and unexplained hypokalemia.
Treatment is dependent on the underlying cause and
includes surgery and drug therapy to normalize hormone
levels.
Nursing care revolves around the risk of infection,
imbalanced nutrition, disturbed self-esteem, risk of injury,
and impaired skin integrity.
Lifetime hormone therapy is required by patients who
undergo adrenalectomy or hypophysectomy. Care
instructions are based on patients inability to react
physiologically to a stressor.
Adrenocortical Insufficiency
Primary hypofunction of the adrenal cortex, or
Addisons disease, results in a reduction of all three
classes of adrenal corticosteroids (glucocorticoids,
 mineralocorticoids, and androgens). Secondary disease
results from pituitary dysfunction.
The most common cause in the United States is
autoimmune, where the adrenal cortex is destroyed by
autoantibodies.
Manifestations have a slow onset and include
weakness, weight loss, and anorexia. Due to increased ACTH,
skin hyperpigmentation is seen in exposed and unexposed
areas of the body, at pressure points, over joints, and in
palmar creases.
Treatment is hormone therapy. Hydrocortisone, the
most commonly used form of hormone therapy, has both
glucocorticoid and mineralocorticoid properties. During times
of stress, glucocorticoid dosage is increased to prevent
Addisonian crisis.
Mineralocorticoid replacement with fludrocortisone
acetate (Florinef) is given daily with increased dietary salt.
NURSING MANAGEMENT: ADDISONS DISEASE
When the patient with Addisons disease is
hospitalized, frequent nursing assessment is necessary. It is
important to include daily weights, corticosteroid
administration, protection against infection, and assistance
with daily hygiene.
The serious nature of the disease and the need for
lifelong hormone therapy necessitate a carefully presented
teaching plan. Focus your care on helping the patient
maintain hormone balance while managing the medication
regimen, recognizing the need for extra medication, and
techniques for stress management.
It is critical that the patient wear an identification
bracelet and carry an emergency kit at all times.
Addisonian Crisis
Patients with Addisons disease are at risk for acute
adrenal insufficiency, a life-threatening emergency caused
by a sudden decrease in adrenocortical hormones.
It is triggered by stress (e.g., surgery, trauma,
psychologic distress), sudden withdrawal of corticosteroid
hormone therapy, and postadrenal surgery.
 Manifestations include postural hypotension,
tachycardia, dehydration, hyponatremia, hyperkalemia,
hypoglycemia, fever, weakness, and confusion.
Treatment is shock management and high-dose
hydrocortisone replacement. Large volumes of 0.9% saline
solution and 5% dextrose are given to reverse hypotension
and electrolyte imbalances until blood pressure (BP)
normalizes.
Complications Associated with Corticosteroid Therapy
The use of long-term corticosteroids in therapeutic
doses often leads to serious complications and side effects
such as risk of infection, osteoporosis, gastric ulceration, and
alteration in fluid and electrolytes balance.
Therapy is reserved for diseases in which there is a risk
of death or permanent loss of function, and conditions in
which short-term therapy is likely to produce remission or
recovery. Potential treatment benefits must always be
weighed against risks.
The danger of abrupt cessation of corticosteroid
therapy must be emphasized to patients and significant
others.
Corticosteroids taken longer than 1 week will suppress
adrenal production, and oral corticosteroids should be
tapered.
Ensure that increased doses of corticosteroids are
prescribed in acute care or home care situations with
increased physical or emotional stress.
HYPERALDOSTERONISM
Hyperaldosteronism is characterized by excessive
aldosterone secretion commonly caused by small solitary
adrenocortical adenoma.
The main effects are sodium retention and potassium
and hydrogen ion excretion, resulting in hypertension with
hypokalemic alkalosis.
The preferred treatment is surgical removal of adenoma
(adrenalectomy).
Patients with bilateral adrenal hyperplasia are treated
with drugs including potassiumsparing diuretics. Calcium
 channel blockers may be used to control BP.
Patients are taught to monitor their own BP along with
the importance of monitoring.
PHEOCHROMOCYTOMA
A pheochromocytoma is a rare condition
characterized by an adrenal medulla tumor that produces
excessive catecholamines (epinephrine, norepinephrine),
resulting in severe hypertension.
Manifestations include severe, episodic hypertension
accompanied by classic triad of (1) severe, pounding
headache, (2) tachycardia with palpitations and profuse
sweating, and (3) unexplained abdominal or chest pain.
Attacks may be provoked by many medications,
including antihypertensives, opioids, radiologic contrast
media, and tricyclic antidepressants.
If undiagnosed and untreated, pheochromocytoma may
lead to diabetes mellitus, cardiomyopathy, and death.
Treatment consists of surgical removal of tumor.