Endocrine System Lecture

Learning Objectives:
At the end of this lecture, you will be able to:
1. Describe the functions of each of the endocrine
glands and their hormones.
2. Identify the diagnostic tests used to determine
alterations in function of each of the endocrine
glands.
3. Compare hypothyroidism and hyperthyroidism: their
causes, clinical manifestations, management, and
nursing interventions.
JOFRED M. MARTINEZ, RN

4. Develop a plan of nursing care for the patient
undergoing thyroidectomy.
5. Compare hyperparathyroidism & hypoparathyroidism
their causes, clinical manifestations, management,
and nursing interventions.
6. Compare Addison’s disease with Cushing’s
syndrome: their causes, clinical manifestations,
management, and nursing interventions.
7. Use the nursing process as a framework for care of
patients with adrenal insufficiency.

8. Use the nursing process as a framework for care of
patients with Cushing’s syndrome.
9. Identify the teaching needs of patients requiring
corticosteroid therapy.

Hormones
• chemical substances secreted by the endocrine
glands.
• help to regulate organ function in relation with
the nervous system
• mechanism for regulating hormone
concentration in the bloodstream is called
negative feedback

Chemistry of Hormones
Hormones are classified into three groups:
1. AMINES - structural variations of the amino
acid tyrosine.
e.g. thyroxine from the thyroid gland and epinephrine
and norepinephrine from the adrenal medulla
2. PROTEINS - these hormones are chains of
amino acids.
e.g. insulin from the pancreas, growth hormone from
the anterior pituitary gland, and calcitonin from the
thyroid gland

Chemistry of Hormones
3. STEROIDS - cholesterol is the precursor for
the steroid hormones
e.g. cortisol and aldosterone from the adrenal cortex,
estrogen and progesterone from the ovaries, and
testosterone from the testes.

Work of Hormones
1. HORMONAL MECHANISM
The hypothalamus secretes hormones that
stimulate the anterior pituitary gland to secrete
hormones that stimulate other endocrine
glands to secrete hormones.

Work of Hormones
2. HUMORAL MECHANISM
Capillary blood contains a low concentration of
calcium that stimulates secretion of parathyroid
hormone.
3. NEURAL MECHANISM
Preganglionic SNS fiber stimulates the adrenal
medulla cells to secrete catecholamines.

Regulation of Hormones
NEGATIVE
FEEDBACK
SYSTEM

Hypothalamus
HYPOTHALAMUS
• small region of the brain below the thalamus
and is the major link between the nervous and
endocrine systems.

Hypothalamus
HYPOTHALAMUS
Releasing and inhibiting hormones
1. Corticotropin-Releasing Hormone (CRH)
2. Thyrotropin-Releasing Hormone (TRH)
3. Growth hormone-Releasing Hormone (GHRH)
4. Gonadotropin-Releasing Hormone (GnRH)
• Controls the release of pituitary hormones

Pituitary Gland
• The pituitary gland, or the hypophysis, is a
round structure about 1.27 cm (1⁄2 inch) in
diameter located on the inferior aspect of the
brain.
• It is divided into the anterior, intermediate, and
posterior lobes.
• Commonly referred to as the master gland, the
pituitary secretes hormones that control the
secretion of hormones by other endocrine
glands

Major Actions and Source of Hormones
ANTERIOR PITUITARY
1. Growth hormone (GH)
• Stimulates growth of bone and muscle, promotes
protein synthesis and fat metabolism, decreases
carbohydrate metabolism
2. Adrenocorticotropic hormone (ACTH)
• Stimulates synthesis and secretion of adrenal cortical
hormones
3. Thyroid-stimulating hormone (TSH)
• Stimulates synthesis and secretion of thyroid hormone

ANTERIOR PITUITARY
4. Follicle-stimulating hormone (FSH)
• Female: stimulates growth of ovarian follicle, ovulation
• Male: stimulates sperm production
5. Luteinizing hormone (LH)
• Female: stimulates development of corpus luteum,
release of oocyte, production of estrogen and
progesterone
• Male: stimulates secretion of testosterone,
development of interstitial tissue of testes

POSTERIOR PITUITARY
1. Antidiuretic hormone (ADH)
• Increases water reabsorption by kidney
2. Oxytocin
• Stimulates contraction of pregnant uterus, milk
ejection from breasts after childbirth
If you are a breast-feeding mom, hearing your
baby cry, thinking about your baby, or smelling
your baby can cause the letdown reflex to occur.

Hypopituitarism
HYPOPITUITARISM
• results from disease of the pituitary gland itself
or of the hypothalamus
• results from destruction of the anterior lobe of
the pituitary gland
Panhypopituitarism (Simmonds’ disease) is total
absence of all pituitary secretions.
Postpartum pituitary necrosis (Sheehan’s
syndrome) is another uncommon cause of failure of
the anterior pituitary.

Hypopituitarism
Hypopituitarism is also a complication of:
• radiation therapy to the head and neck area
• total destruction of the pituitary gland by
trauma, tumor, or vascular lesion that removes
all stimuli that are normally received by the
thyroid, the gonads, and the adrenal glands.

Hypopituitarism
The result of hypopituitarism is:
 Extreme weight loss
 Emaciation
 Hair loss
 Impotence
 Amenorrhea
 Hypometabolism
 Hypoglycemia
 Atrophy of all endocrine glands and organs
Coma and death occur if the missing hormones are
not replaced.

Pituitary Tumors
• Pituitary tumors are usually benign, although
their location and effects on hormone
production by target organs can cause life
threatening effects.
• Three principal types of pituitary tumors is
represented by an overgrowth of:
 eosinophilic cells
 basophilic cells
 chromophobic cells

Pituitary Tumors (Manifestations)
• Eosinophilic tumors that develop early in life
result in GIGANTISM.
• Basophilic tumors give rise to CUSHING’S
SYNDROME with features largely attributable
to hyperadrenalism, including masculinization
and amenorrhea in females, truncal obesity,
hypertension, osteoporosis, and polycythemia.
• Chromophobic tumors usually produce no
hormones but destroy the rest of the pituitary
gland, causing HYPOPITUITARISM.

Assessment and Diagnostic Findings
• COMPUTED TOMOGRAPHY (CT) and
MAGNETIC RESONANCE IMAGING (MRI)
are used to diagnose the presence and extent
of pituitary tumors.
• Serum levels of pituitary hormones may be
obtained along with measurements of
hormones of target organs (eg, thyroid,
adrenal) to assist in diagnosis if other
information is inconclusive.

Medical / Surgical Management
• Surgical removal of the pituitary tumor through a
transsphenoidal approach is the usual treatment.
• STEREOTACTIC RADIATION THERAPY, which
requires use of a neurosurgery-type stereotactic
frame, may be used to deliver external-beam
radiation.
• Other treatments include conventional radiation
therapy, bromocriptine (dopamine antagonist), and
octreotide (synthetic analog of growth hormone).

Medical / Surgical Management
• HYPOPHYSECTOMY, or removal of the pituitary
gland, is the treatment of choice in patients with
Cushing’s syndrome due to excessive production
of ACTH by a tumor of the pituitary gland.
• Menstruation ceases and infertility occurs after
total or near-total ablation of the pituitary gland.
Replacement therapy with CORTICOSTEROIDS
and THYROID HORMONE is necessary.

• Diabetes insipidus is a disorder of the posterior lobe of
the pituitary gland characterized by a deficiency of
antidiuretic hormone (ADH), or vasopressin.
• Great thirst (polydipsia) and large volumes of dilute
urine characterize the disorder.
• It may be secondary to head trauma, brain tumor,
infections of the central nervous system, tumors or
surgical ablation or irradiation of the pituitary gland.
Diabetes insipidus (DI) has nothing to do with
blood sugar. Diabetes mellitus (DM) has
everything to do with blood sugar.
Diabetes Insipidus

Diabetes Insipidus
• Another cause of diabetes insipidus is failure of
the renal tubules to respond to ADH; this
nephrogenic form may be related to
hypokalemia, hypercalcemia, and a variety of
medications (eg, lithium).
The only electrolyte that is affected by the amount
of water in the vascular space is sodium. If the
water level in the blood is too high, the sodium
level will go down. If the water level in the blood is
too low, the sodium level will go up.

Diabetes Insipidus (Manifestations)
• enormous daily output of very dilute, water-like urine
 specific gravity of 1.001 to 1.005
 contains no abnormal substances such as glucose
and albumin
• intense thirst, the patient tends to drink 2 to 20 liters
of fluid daily and craves cold water.
Attempts to restrict fluids cause the patient to
experience an insatiable craving for fluid and to
develop hypernatremia and severe dehydration.

Assessment and Diagnostic Finding
• The FLUID DEPRIVATION TEST is carried out by
withholding fluids for 8 to 12 hours or until 3% to 5%
of the body weight is lost. The patient is weighed
frequently during the test. Plasma and urine
osmolality studies are performed at the beginning
and end of the test.
• Concurrent measurements of plasma levels of ADH
(vasopressin) and plasma and urine osmolality, a
trial of DESMOPRESSIN (synthetic vasopressin)
therapy and intravenous infusion of hypertonic saline
solution.

Medical Management
The objectives of therapy are:
1. To replace ADH (which is usually a long-term
therapeutic program)
2. To ensure adequate fluid replacement
3. To identify and correct the underlying intracranial
pathology.

Pharmacologic Management
• DESMOPRESSIN (DDAVP), is administered
intranasally; the patient sprays the solution into the
nose through a flexible calibrated plastic tube. One
or two administrations daily or every 12 to 24 hours
usually control the symptoms.
• Intramuscular administration of ADH, or
VASOPRESSIN TANNATE IN OIL. It is administered
every 24 to 96 hours. The vial of medication should
be warmed or shaken vigorously before
administration. The injection is administered in the
evening so that maximum results are obtained
during sleep.

Pharmacologic Management
• Clofibrate, a hypolipidemic agent, given on patients
with diabetes insipidus who have some residual
hypothalamic vasopressin.
• Chlorpropamide (Diabinese) and thiazide diuretics
are also used in mild forms of the disease because
they potentiate the action of vasopressin.
The patient receiving chlorpropamide should be
warned of the possibility of hypoglycemic
reactions.

Nursing Management
• Provide encouragement and support while the patient is
undergoing studies for a possible cranial lesion.
• Inform the patient and family about follow-up care and
emergency measures.
• Provide specific verbal and written instructions, show the
patient how to administer the medications, and observe
return demonstrations as appropriate.
• Advise the patient to wear a medical identification
bracelet and to carry medication and information about
this disorder at all times.
Vasopressin must be administered with caution if the
patient has coronary artery disease because the
medication causes vasoconstriction.

Syndrome of Inappropriate ADH
• SYNDROME OF INAPPROPRIATE ANTIDIURETIC
HORMONE (SIADH) secretion includes excessive
growth hormone (ADH) secretion from the pituitary
gland even in the face of subnormal serum
osmolality.
• Patients with this disorder cannot excrete a dilute
urine. They retain fluids and develop a sodium
deficiency known DILUTIONAL HYPONATREMIA.

SIADH
• Disorders of the central nervous system, such as
head injury, brain surgery or tumor, and infection, are
thought to produce SIADH by direct stimulation of
the pituitary gland.
• Some medications (vincristine, phenothiazines,
tricyclic antidepressants, thiazide diuretics, and
others) and nicotine have been implicated in SIADH;
they either directly stimulate the pituitary gland or
increase the sensitivity of renal tubules to circulating
ADH.

Medical Management
• Eliminating the underlying cause, if possible, and
restricting fluid intake.
• Diuretics (eg, furosemide [Lasix]) may be used along
with fluid restriction if severe hyponatremia is
present.
• Close monitoring of fluid intake and output, daily
weight, urine and blood chemistries, and neurologic
status
• Supportive measures and explanations of
procedures and treatments assist the patient to deal
with this disorder

Review!
Not enough ADH Diabetes Insipidus (DI).
Too much ADH Syndrome of
Inappropriate ADH secretion (SIADH).

Anatomy & Physiology
• butterfly-shaped organ consists of two lateral
lobes connected by an isthmus located in the
lower neck anterior to the trachea
• about 5 cm long and 3 cm wide and weighs
about 30 g
• blood flow to the thyroid is very high (about 5
mL/min per gram of thyroid tissue), about five
times the blood flow to the liver

THYROID (FOLLICULAR CELLS)
Thyroid hormones:
1. Triiodothyronine (T3)
2. Thyroxine (T4)
• Increase the metabolic rate; increase protein and
bone turnover; increase responsiveness to
catecholamines; necessary for fetal and infant
growth and development

THYROID C CELLS
1. Calcitonin
• Lowers blood calcium and phosphate levels

Role of Iodine
• essential to the thyroid gland for synthesis of its
hormones
• thyroid gland is extremely efficient in taking up
iodide from the blood and concentrating it within
the cells, where iodide ions are converted to
iodine molecules, which react with tyrosine (an
amino acid) to form the thyroid hormones

Regulation of Thyroid Hormone
HYPOTHALAMIC-PITUITARY-THYROID AXIS

Thyroid Function Tests
• laboratory measurement of thyroid hormones
 serum immunoassay for TSH and free
thyroxine (FT4)
• thyroid scanning
• biopsy
• ultrasonography

Current recommendations suggest
TSH screening for all adults beginning at age 35, and every 5 years
thereafter
Thyroid Stimulating Hormone
• Measurement of the serum TSH concentration
is the single best screening test of thyroid
function because of its high sensitivity.
• Values above the normal range of 0.4 to 6.15
μU/mL indicate primary hypothyroidism, and
low values indicate hyperthyroidism.
Current recommendations suggest TSH screening
for all adults beginning at age 35, and every 5 years
thereafter.

thereafter
Serum Free Thyroxine
• The test most commonly used to confirm an
abnormal TSH is FT4.
• FT4 is a direct measurement of free (unbound)
thyroxine, the only metabolically active fraction
of T4. The range of FT4 in serum is normally
0.9 to 1.7 ng/dL (11.5 to 21.8 pmol/L).

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Serum T3 and T4
• Measurement of total T3 or T4 includes
protein-bound and free hormone levels that
occur in response to TSH secretion.
• Normal range for T4 is 4.5 to 11.5 μg/dL (58.5
to 150 nmol/L).
• The normal range for serum T3 is 70 to 220
μg/dL (1.15 to 3.10 nmol/L).

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T3 Resin Uptake Test
• The T3 resin uptake test is an indirect measure
of unsaturated TBG.
• Its purpose is to determine the amount of
thyroid hormone bound to TBG and the
number of available binding sites.
• The normal T3 uptake value is 25% to 35%
(relative uptake fraction, 0.25 to 0.35), which
indicates that about one third of the available
sites of TBG are occupied by thyroid hormone.

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Thyroid Antibodies
• Antithyroid antibody titers are normally present in
5% to 10% of the population and increase with
age.
Radioactive Iodine Uptake
• The radioactive iodine uptake test measures the
rate of iodine uptake by the thyroid gland.
• It measures the proportion of the administered
dose present in the thyroid gland at a specific time
after its administration.

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Fine Needle Aspiration Biopsy
• It is often the initial test for evaluation of thyroid
masses.
• Results are reported as:
1. negative (benign)
2. positive (malignant)
3. indeterminate (suspicious)
4. inadequate (nondiagnostic)

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Thyroid Scan, Radioscan, and Scintiscan
• In a thyroid scan, a scintillation detector or gamma
camera moves back and forth across the area to be
studied in a series of parallel tracks, and a visual
image is made of the distribution of radioactivity in
the area being scanned.
• Scans are helpful in determining the location, size,
shape, and anatomic function of the thyroid gland,
particularly when thyroid tissue is substernal or
large.

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Other Diagnostic Tests
• Ultrasound, CT scans, and MRI may be used to
clarify or confirm the results of other diagnostic
studies.
• Thyroglobulin (Tg), a precursor for T3 and T4,
can be measured reliably in the serum by
radioimmunoassay.

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Nursing Implications
• When thyroid tests are scheduled, it is necessary to
determine whether the patient has taken
medications or agents that contain iodine because
these may alter the test results.
• Sources of iodine are topical antiseptics,
multivitamin preparations, and food supplements
frequently found in health food stores; cough syrups;
and amiodarone, an antiarrhythmic agent.
• Other medications that may affect test results are
estrogens, salicylates, amphetamines,
chemotherapeutic agents, antibiotics,
corticosteroids, and mercurial diuretics.

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Abnormal Thyroid Function
• Inadequate secretion of thyroid hormone during
fetal and neonatal development results in stunted
physical and mental growth because of general
depression of metabolic activity.
• In adults, hypothyroidism manifests as lethargy,
slow mentation, and generalized slowing of body
functions.
Myxedema is the worst-case scenario of
hypothyroidism. If a test question says
“myxedema,” think hypothyroidism.

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Hypothyroidism
• Hypothyroidism results from suboptimal levels of thyroid
hormone.
• Thyroid deficiency can affect all body functions and can
range from mild, subclinical forms to myxedema, an
advanced form.
• The most common cause of hypothyroidism in adults is
autoimmune thyroiditis (Hashimoto’s disease), in which
the immune system attacks the thyroid gland.

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Clinical Manifestations
• Early symptoms of hypothyroidism are nonspecific, but
extreme fatigue makes it difficult for the person to
complete a full day’s work or participate in usual
activities.
• Reports of hair loss, brittle nails, and dry skin are
common, and numbness and tingling of the fingers may
occur.
• On occasion, the voice may become husky, and the
patient may complain of hoarseness.
• Menstrual disturbances such as menorrhagia or
amenorrhea occur, in addition to loss of libido.

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• Hypothyroidism affects women five times more
frequently than men and occurs most often between 30
and 60 years of age.
• Severe hypothyroidism results in a subnormal
temperature and pulse rate.
• The patient usually begins to gain weight even without
an increase in food intake, although severely
hypothyroid patients may be cachectic.
• The skin becomes thickened because of an
accumulation accumulation of mucopolysaccharides in
the subcutaneous tissues.

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• The hair thins and falls out; the face becomes
expressionless and masklike.
• The patient often complains of being cold even in a
warm environment.
• At first, the patient may be irritable and may complain of
fatigue, but as the condition progresses, the emotional
responses are subdued.
• The mental processes become dulled, and the patient
appears apathetic.
• Speech is slow, the tongue enlarges, and hands and
feet increase in size.

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• The patient frequently complains of constipation.
• Deafness may also occur.
• Advanced hypothyroidism may produce personality and
cognitive changes characteristic of dementia.
• Inadequate ventilation and sleep apnea can occur with
severe hypothyroidism.
• Pleural effusion, pericardial effusion, and respiratory
muscle weakness may also occur.
• Severe hypothyroidism is associated with an elevated
serum cholesterol level, atherosclerosis, coronary artery
disease, and poor left ventricular function.

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• The patient with advanced hypothyroidism is
hypothermic and abnormally sensitive to sedatives,
opioids, and anesthetic agents.
• Patients with unrecognized hypothyroidism who are
undergoing surgery are at increased risk for
intraoperative hypotension and postoperative heart
failure and altered mental status.
• Myxedema coma describes the most extreme, severe
stage of hypothyroidism, in which the patient is
hypothermic and unconscious.
• Myxedema coma may follow increasing lethargy,
progressing to stupor and then coma.

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• The patient’s respiratory drive is depressed, resulting in
alveolar hypoventilation, progressive CO2 retention,
narcosis, and coma.
• These symptoms, along with cardiovascular collapse
and shock, require aggressive and intensive therapy if
the patient is to survive.
• Even with early vigorous therapy, however, mortality is
high.

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Medical Management
PHARMACOLOGIC THERAPY
• Synthetic levothyroxine (Synthroid or Levothroid) is the
preferred preparation for treating hypothyroidism and
suppressing nontoxic goiters.
• Desiccated thyroid is used less frequently because it
often results in transient elevated serum concentrations
of T3, with occasional symptoms of hyperthyroidism.

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Medical Management
PREVENTION OF CARDIAC DYSFUNCTION
• Any patient who has had hypothyroidism for a long
period is almost certain to have elevated serum
cholesterol levels, atherosclerosis, and coronary artery
disease.
• The occurrence of angina is the signal that the oxygen
needs of the myocardium exceed its blood supply.
• Angina or dysrhythmias may occur when thyroid
replacement is initiated because thyroid hormones
enhance the cardiovascular effects of catecholamines.

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Medical Management
PREVENTION OF CARDIAC DYSFUNCTION
• Angina or dysrhythmias may occur when thyroid
replacement is initiated because thyroid hormones
enhance the cardiovascular effects of catecholamines.
• If angina or dysrhythmias occur, thyroid hormone
administration must be discontinued immediately.
• Later, when it can be resumed safely, thyroid hormone
replacement should be prescribed cautiously at a lower
dosage and under the close observation of the physician
and the nurse.

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Medical Management
PREVENTION OF MEDICATION INTERACTIONS
• Thyroid hormones may increase blood glucose levels,
which may necessitate adjustment in the dosage of insulin
or oral antidiabetic agents in patients with diabetes.
• The effects of thyroid hormone may be increased by
phenytoin (Dilantin) and tricyclic antidepressant agents.
• Thyroid hormones may also increase the pharmacologic
effects of digitalis glycosides, anticoagulant agents, and
indomethacin, requiring careful observation and
assessment by the nurse for side effects.
• Bone loss and osteoporosis may also occur with thyroid
therapy.

SUPPORTIVE THERAPY
In severe hypothyroidism and myxedema coma, management
includes maintaining vital functions. Arterial blood gases may be
measured to determine CO2 retention and to guide the use of
assisted ventilation to combat hypoventilation. Pulse oximetry
may also be helpful in monitoring oxygen saturation levels. Fluids
are administered cautiously because of the danger of water intoxication.
Application of external heat (eg, heating pads) is avoided
because it increases oxygen requirements and may lead to vascular
collapse. If hypoglycemia is evident, concentrated glucose
may be prescribed to provide glucose without precipitating fluid
overload. Thyroid hormone (usually Synthroid) is administered
intravenously until consciousness is restored if myxedema has
progressed to myxedema coma. The patient is then continued on
oral thyroid hormone therapy. Because of an associated adrenocortical
insufficiency, corticosteroid therapy may be necessary.
Medical Management
SUPPORTIVE THERAPY
• In severe hypothyroidism and myxedema coma,
management includes maintaining vital functions.
• Arterial blood gases may be measured to determine CO2
retention and to guide the use of assisted ventilation to
combat hypoventilation.
• Pulse oximetry may also be helpful in monitoring oxygen
saturation levels.
• Fluids are administered cautiously because of the danger
of water intoxication.
• Application of external heat is avoided because it increases
oxygen requirements and may lead to vascular collapse.

SUPPORTIVE THERAPY
Medical Management
SUPPORTIVE THERAPY
• If hypoglycemia is evident, concentrated glucose may be
prescribed to provide glucose without precipitating fluid
overload.
• Thyroid hormone (usually Synthroid) is administered
intravenously until consciousness is restored if
myxedema has progressed to myxedema coma.
• The patient is then continued on oral thyroid hormone
therapy.
• Because of an associated adrenocortical insufficiency,
corticosteroid therapy may be necessary.

SUPPORTIVE THERAPY
Nursing Management
MODIFYING ACTIVITY
• The patient with hypothyroidism experiences decreased
energy and moderate to severe lethargy. As a result, the
risk for complications from immobility increases.
• The patient’s ability to exercise and participate in
activities is further limited by the changes in
cardiovascular and pulmonary status secondary to
hypothyroidism.
• A major role of the nurse is assisting with care and
hygiene while encouraging the patient to participate in
activities within established tolerance levels to prevent
the complications of immobility.

SUPPORTIVE THERAPY
Nursing Management
MONITORING PHYSICAL STATUS
• The nurse closely monitors the patient’s vital signs and
cognitive level to detect the following:
 Deterioration of physical and mental status
 Signs and symptoms indicating that treatment has
resulted in the metabolic rate exceeding the ability of
the cardiovascular and pulmonary systems to respond
 Continued limitations or complications of myxedema

SUPPORTIVE THERAPY
Nursing Management
PROMOTING PHYSICAL COMFORT
• The patient often experiences chilling and extreme
intolerance to cold, even if the room feels comfortable or
hot to others.
• Extra clothing and blankets are provided, and the patient
is protected from drafts.
• Use of heating pads and electric blankets is avoided
because of the risk of peripheral vasodilation, further
loss of body heat, and vascular collapse.
• Additionally, the patient could be burned by these items
without being aware of it because of delayed responses
and decreased mental status.

SUPPORTIVE THERAPY
In
Nursing Management
PROVIDING EMOTIONAL SUPPORT
• The patient with moderate to severe hypothyroidism may
experience severe emotional reactions to changes in
appearance and body image and the frequent delay in
diagnosis.
• As hypothyroidism is treated successfully and symptoms
subside, the patient may experience depression and
guilt as a result of the progression and severity of
symptoms that occurred.
• The nurse informs the patient and family that the
symptoms and inability to recognize them are common
and part of the disorder itself.

SUPPORTIVE THERAPY
In
Nursing Management
PROVIDING EMOTIONAL SUPPORT
• The patient and family may require assistance and
counseling to deal with the emotional concerns and
reactions that result.

SUPPORTIVE THERAPY
In
Hyperthyroidism
• Graves’ disease, results from an excessive output of
thyroid hormones caused by abnormal stimulation of the
thyroid gland by circulating immunoglobulins.
• It may appear after an emotional shock, stress, or an
infection, but the exact significance of these relationships is
not understood.
• Other common causes of hyperthyroidism include
thyroiditis and excessive ingestion of thyroid hormone.
Hyperthyroidism is mainly seen in females and is
most common after childbirth or during
menopause.

SUPPORTIVE THERAPY
In
• Patients with well-developed hyperthyroidism exhibit a
characteristic group of signs and symptoms
(thyrotoxicosis).
• The presenting symptom is often nervousness.
• These patients are often emotionally hyperexcitable,
irritable, and apprehensive; they cannot sit quietly; they
suffer from palpitations; and their pulse is abnormally
rapid at rest as well as on exertion.
• They tolerate heat poorly and perspire unusually freely.
• The skin is flushed continuously, with a characteristic
salmon color, and is likely to be warm, soft, and moist.

SUPPORTIVE THERAPY
In
• Elderly patients, however, may report dry skin and diffuse
pruritus. A fine tremor of the hands may be observed.
• Patients may exhibit exophthalmos, which produces a
startled facial expression.
• Other manifestations include an increased appetite and
dietary intake, progressive weight loss, abnormal muscular
fatigability and weakness, amenorrhea, and changes in
bowel function.
• The pulse rate ranges constantly between 90 and 160
beats/min; the systolic, but characteristically not the
diastolic, blood pressure is elevated; atrial fibrillation may
occur; and cardiac decompensation in the form of heart
failure is common, especially in elderly patients.

SUPPORTIVE THERAPY
In
• Osteoporosis and fracture are also associated with
hyperthyroidism.
• Cardiac effects may include sinus tachycardia or
dysrhythmias, increased pulse pressure, and
palpitations; it has been suggested that these changes
may be related to increased sensitivity to
catecholamines or to changes in neurotransmitter
turnover.
• Myocardial hypertrophy and heart failure may occur if
the hyperthyroidism is severe and untreated.
• The course of the disease may be mild, characterized by
remissions and exacerbations and terminating with
spontaneous recovery in a few months or years.

SUPPORTIVE THERAPY
In
• Conversely, it may progress relentlessly, with the
untreated person becoming emaciated, intensely
nervous, delirious, and even disoriented; eventually, the
heart fails.

SUPPORTIVE THERAPY
In
• The thyroid gland invariably is enlarged to some extent.
• It is soft and may pulsate; a thrill often can be palpated,
and a bruit is heard over the thyroid arteries.
• In advanced cases, the diagnosis is made on the basis
of the symptoms and an increase in serum T4 and an
increased 123I or 125I uptake by the thyroid in excess of
50%.

SUPPORTIVE THERAPY
In
Thyroid Storm
• Thyroid storm (thyrotoxic crisis) is a form of severe
hyperthyroidism, usually of abrupt onset.
• Untreated it is almost always fatal, but with proper
treatment the mortality rate is reduced substantially.
• The patient with thyroid storm or crisis is critically ill and
requires astute observation and aggressive and
supportive nursing care during and after the acute stage
of illness.

SUPPORTIVE THERAPY
In
Thyroid Storm
Thyroid storm is characterized by:
• High fever (hyperpyrexia) above 38.5°C
• Extreme tachycardia (more than 130 beats/min)
• Exaggerated symptoms of hyperthyroidism with
disturbances of a major system—for example, GI
(weight loss, diarrhea, abdominal pain), or
cardiovascular (edema, chest pain, dyspnea,
palpitations)
• Altered neurologic or mental state, which frequently
appears as delirium psychosis, somnolence, or coma

SUPPORTIVE THERAPY
In
Thyroid Storm
• Life-threatening thyroid storm is usually precipitated by
stress, such as injury, infection, thyroid and nonthyroid
surgery, tooth extraction, insulin reaction, diabetic
acidosis, pregnancy, digitalis intoxication, abrupt
withdrawal of antithyroid medications, extreme
emotional stress, or vigorous palpation of the thyroid.
• These factors can precipitate thyroid storm in the
partially controlled or completely untreated patient with
hyperthyroidism.

SUPPORTIVE THERAPY
In
Thyroid Storm
MANAGEMENT
• Immediate objectives are reduction of body temperature
and heart rate and prevention of vascular collapse.
Measures to accomplish these objectives include:
• A hypothermia mattress or blanket, ice packs, a cool
environment, hydrocortisone, and acetaminophen
(Tylenol).
• Salicylates (eg, aspirin) are not used because they
displace thyroid hormone from binding proteins and
worsen the hypermetabolism.
• Humidified oxygen is administered to improve tissue
oxygenation and meet the high metabolic demands.

SUPPORTIVE THERAPY
In
Thyroid Storm
MANAGEMENT
• Arterial blood gas levels or pulse oximetry may be used to
monitor respiratory status.
• Intravenous fluids containing dextrose are administered to
replace liver glycogen stores that have been decreased in
the hyperthyroid patient.
• PTU or methimazole is administered to impede formation
of thyroid hormone and block conversion of T4 to T3, the
more active form of thyroid hormone.
• Hydrocortisone is prescribed to treat shock or adrenal
insufficiency.
• Iodine is administered to decrease output of T4 from the
thyroid gland.

SUPPORTIVE THERAPY
In
Thyroid Storm
MANAGEMENT
• For cardiac problems such as atrial fibrillation,
dysrhythmias, and heart failure, sympatholytic agents
may be administered.
• Propranolol, combined with digitalis, has been effective
in reducing severe cardiac symptoms.

SUPPORTIVE THERAPY
In
Medical Management
• Treatment of hyperthyroidism is directed toward reducing
thyroid hyperactivity to relieve symptoms and remove the
cause of important complications.
• Two forms of pharmacotherapy are available for treating
hyperthyroidism and controlling excessive thyroid activity:
1. use of irradiation by administration of the radioisotope
123I or 131I for destructive effects on the thyroid gland
and
2. antithyroid medications that interfere with the synthesis
of thyroid hormones and other agents that control
manifestations of hyperthyroidism.

SUPPORTIVE THERAPY
In
Medical Management
RADIOACTIVE IODINE THERAPY
• The goal of radioactive iodine therapy (123I or 131I) is to
destroy the overactive thyroid cells.
• The patient is instructed about what to expect with this
tasteless, colorless radioiodine, which may be
administered by the radiologist.
• About 70% to 85% of patients are cured by one dose of
radioactive iodine.
• The patient is observed for signs of thyroid storm;
propranolol is useful in controlling these symptoms.

SUPPORTIVE THERAPY
In
Medical Management
RADIOACTIVE IODINE THERAPY
• Radioactive iodine has been used to treat toxic
adenomas and multinodular goiter and most varieties of
thyrotoxicosis; it is preferred for treating patients beyond
the childbearing years with diffuse toxic goiter.
• It is contraindicated in pregnancy and in nursing mothers
because radioiodine crosses the placenta and is
secreted in breast milk.
• A major advantage of treatment with radioactive iodine is
that it avoids many of the side effects associated with
antithyroid medications.

SUPPORTIVE THERAPY
In
Medical Management
ANTITHYROID MEDICATIONS
• Antithyroid agents block the utilization of iodine by
interfering with the iodination of thyrosine and the
coupling of iodothyrosines in the synthesis of thyroid
hormones.
• The most commonly used medications are
propylthiouracil (Propacil, PTU) or methimazole
(Tapazole) until the patient is euthyroid (ie, neither
hyperthyroid nor hypothyroid).
Agranulocytosis can develop as a side effect of the
antithyroid drugs. Signs of this include sore mouth, sore
throat, rash, and fever. A white blood cell count should be
checked prior to initiating therapy.

SUPPORTIVE THERAPY
In
Medical Management
• Toxic complications of antithyroid medications are
relatively uncommon; nevertheless, the importance of
periodic follow-up is emphasized because medication
sensitization, fever, rash, urticaria, or even
agranulocytosis and thrombocytopenia may develop.
• With any sign of infection, especially pharyngitis and
fever or the occurrence of mouth ulcers, the patient is
advised to stop the medication, notify the physician
immediately, and undergo hematologic studies.

SUPPORTIVE THERAPY
In
Medical Management
• Patients taking antithyroid medications are instructed not to
use decongestants for nasal stuffiness because they are
poorly tolerated.
• Antithyroid medications are contraindicated in late
pregnancy because they may produce goiter and cretinism
in the fetus.
• Thyroid hormone is available as thyroglobulin (Proloid) and
levothyroxine sodium (Synthroid). These slow-acting
preparations take about 10 days to achieve their full effect.
• Liothyronine sodium (Cytomel) has a more rapid onset, and
its action is of short duration.

SUPPORTIVE THERAPY
In
Medical Management
ADJUNCTIVE THERAPY
• Iodine or iodide compounds, decrease the release of
thyroid hormones from the thyroid gland and reduce the
vascularity and size of the thyroid.
• Compounds such as potassium iodide (KI), Lugol’s
solution, and saturated solution of potassium iodide
(SSKI) may be used in combination with antithyroid
agents or beta-adrenergic blockers to prepare the
patient with hyperthyroidism for surgery.
There are two types of iodine: dietary iodine and
medicinal iodine. They each have totally different
actions.

SUPPORTIVE THERAPY
In
Medical Management
ADJUNCTIVE THERAPY
• These agents reduce the activity of the thyroid hormone
and the vascularity of the thyroid gland, making the
surgical procedure safer.
• Solutions of iodine and iodide compounds are more
palatable in milk or fruit juice and are administered through
a straw to prevent staining of the teeth.
• Beta-adrenergic blocking agents are important in
controlling the sympathetic nervous system effects of
hyperthyroidism.
Asthmatics and diabetics should not be given beta-
blockers. Beta-blockers can cause bronchospasm
and mask the signs of hypoglycemia.

SUPPORTIVE THERAPY
In
Medical Management
SURGICAL MANAGEMENT
• Surgery is reserved in pregnant women allergic to
antithyroid medications, patients with large goiters, or
patients unable to take antithyroid agents.
• The surgical removal of about five sixths of the thyroid
tissue (subtotal thyroidectomy) practically ensures a
prolonged remission in most patients with exophthalmic
goiter.
Be sure to watch for hypocalcemia postop
thyroidectomy, as this electrolyte imbalance can
affect the airway, the heart, and cause seizures!

SUPPORTIVE THERAPY
In
Medical Management
SURGICAL MANAGEMENT
• Its use is reserved for large goiters, presence of
obstructive symptoms, pregnant women, or when there
is a need for rapid normalization of thyroid function.
• Before surgery, propylthiouracil is administered until
signs of hyperthyroidism have disappeared.
• A beta-adrenergic blocking agent (propranolol) may be
used to reduce the heart rate and other signs and
symptoms of hyperthyroidism; however, this does not
create a euthyroid state.

SUPPORTIVE THERAPY
In
Medical Management
SURGICAL MANAGEMENT
• Iodine (Lugol’s solution or potassium iodide) may be
prescribed in an effort to reduce blood loss; however, the
effectiveness of this is unknown.
• Patients receiving iodine medication must be monitored
for evidence of iodine toxicity (iodism), which requires
immediate withdrawal of the medication.
• Symptoms of iodism include swelling of the buccal
mucosa, excessive salivation, coryza, and skin
eruptions.

SUPPORTIVE THERAPY
In
Recurrent Hyperthyroidism
• No treatment for thyrotoxicosis is without side effects,
and all three treatments (radioactive iodine therapy,
antithyroid medications, and surgery) share the same
complications: relapse or recurrent hyperthyroidism and
permanent hypothyroidism.
• The relapse rate after radioactive iodine therapy
depends on the dose used in treatment.
Post radioactive iodine. The client should stay away
from babies, not kiss anyone, and cover the mouth
and nose when coughing and sneezing for 24 hours
after treatment as the iodine can be shed in saliva.

SUPPORTIVE THERAPY
In
Recurrent Hyperthyroidism
• Hypothyroidism occurs in almost 80% of patients at 1
year and in 90% to 100% by 5 years for both the multiple
• low-dose and single high-dose methods.
• Although rates of relapse and the occurrence of
hypothyroidism vary, relapse with antithyroid
medications is about 45% by 1 year after completion of
therapy and almost 75% by 5 years later.
• Discontinuation of antithyroid medications before
therapy is complete usually results in relapse within 6
months in most patients.

SUPPORTIVE THERAPY
In
Thyroiditis
• Thyroiditis, inflammation of the thyroid gland, can be
acute, subacute, or chronic. Each type of thyroiditis is
characterized by inflammation, fibrosis, or lymphocytic
infiltration of the thyroid gland.
ACUTE THYROIDITIS
• Acute thyroiditis is a rare disorder caused by infection of
the thyroid gland by bacteria, fungi, mycobacteria, or
parasites.
• Staphylococcus aureus and other staphylococci are the
most common causes.
• Infection typically causes anterior neck pain and
swelling, fever, dysphagia, and dysphonia.

SUPPORTIVE THERAPY
In
Thyroiditis
• Pharyngitis or pharyngeal pain is often present.
• Examination may reveal warmth, erythema, and
tenderness of the thyroid gland.
• Treatment of acute thyroiditis in includes antimicrobial
agents and fluid replacement.
• Surgical incision and drainage may be needed if an
abscess is present.

SUPPORTIVE THERAPY
In
Thyroiditis
SUBACUTE THYROIDITIS
• Subacute thyroiditis may be subacute granulomatous
thyroiditis (deQuervain’s thyroiditis) or painless
thyroiditis (silent thyroiditis or subacute lymphocytic
thyroiditis).
• Subacute granulomatous thyroiditis is an inflammatory
disorder of the thyroid gland that predominantly affects
women between 40 and 50 years old.
• The condition presents as a painful swelling in the
anterior neck that lasts 1 to 2 months and then
disappears spontaneously without residual effect.

SUPPORTIVE THERAPY
In
Thyroiditis
• The thyroid enlarges symmetrically and may be painful.
• The overlying skin is often reddened and warm.
• Swallowing may be difficult and uncomfortable.
• Irritability, nervousness, insomnia, and weight loss—
manifestations of hyperthyroidism—are common, and
many patients experience chills and fever as well.
• Treatment aims to control the inflammation, nonsteroidal
anti-inflammatory drugs (NSAIDs) are used to relieve
neck pain.

SUPPORTIVE THERAPY
In
Thyroiditis
• Acetylsalicylic acid is avoided if symptoms of
hyperthyroidism occur because aspirin displaces thyroid
hormone from its binding sites and increases the
amount of circulating hormone.
• Beta-blocking agents (eg, propranolol [Inderal]) may be
used to control symptoms of hyperthyroidism.
• Antithyroid agents, which block the synthesis of T3 and
T4, are not effective in thyroiditis because the
associated thyrotoxicosis results from the release of
stored thyroid hormones rather than from their increased
synthesis.

SUPPORTIVE THERAPY
In
Thyroiditis
• In more severe cases, oral corticosteroids may be
prescribed to reduce swelling and relieve pain; however,
they do not usually affect the underlying cause.
• In some cases, temporary hypothyroidism may develop
and may necessitate thyroid hormone therapy.
• Follow-up monitoring is necessary to document the
patient’s return to a euthyroid state.
• Painless thyroiditis (subacute lymphocytic thyroiditis)
often occurs in the postpartum period and is thought to
be an autoimmune process.

SUPPORTIVE THERAPY
In
Thyroiditis
• Treatment is directed at symptoms, and yearly follow-up
is recommended to determine the patient’s need for
treatment of subsequent hypothyroidism.

SUPPORTIVE THERAPY
In
Thyroiditis
CHRONIC THYROIDITIS (HASHIMOTO’S DISEASE)
• Chronic thyroiditis, which occurs most frequently in women
between 30 and 50 years old, has been termed
Hashimoto’s disease, or chronic lymphocytic thyroiditis; its
diagnosis is based on the histologic appearance of the
inflamed gland.
• In contrast to acute thyroiditis, the chronic forms are
usually not accompanied by pain, pressure symptoms, or
fever, and thyroid activity is usually normal or low rather
than increased.
• Cell-mediated immunity may play a significant role in the
pathogenesis of chronic thyroiditis, and there may be a
genetic predisposition to it.

SUPPORTIVE THERAPY
In
Thyroiditis
CHRONIC THYROIDITIS (HASHIMOTO’S DISEASE)
• If untreated, the disease runs a slow, progressive
course, leading eventually to hypothyroidism.
• The objective of treatment is to reduce the size of the
thyroid gland and prevent hypothyroidism.
• Thyroid hormone therapy is prescribed to reduce thyroid
activity and the production of thyroglobulin.
Hashimoto’s thyroiditis can cause hyperthyroidism
or hypothyroidism. The client’s symptoms depend
on which phase of the disease she is in.

SUPPORTIVE THERAPY
In
Thyroid Tumor
• Tumors of the thyroid gland are classified on the basis of
being benign or malignant, the presence or absence of
associated thyrotoxicosis, and the diffuse or irregular
quality of the glandular enlargement.
• If the enlargement is sufficient to cause a visible swelling
in the neck, the tumor is referred to as a goiter.
• All grades of goiter are encountered, from those that are
barely visible to those producing disfigurement.
• Some are symmetric and diffuse; others are nodular.
Some are accompanied by hyperthyroidism, in which
case they are described as toxic; others are associated
with a euthyroid state and are called nontoxic goiters.

SUPPORTIVE THERAPY
In
Endemic Goiter
• The most common type of goiter, encountered chiefly in
geographic regions where the natural supply of iodine is
deficient, is the so-called simple or colloid goiter.
• In addition to being caused by an iodine deficiency,
simple goiter may be caused by an intake of large
quantities of goitrogenic substances in patients with
unusually susceptible glands.
• These substances include excessive amounts of iodine
or lithium, which is used in treating bipolar disorders.
Excessive palpation of a goiter can cause a release
of thyroid hormone that could throw the client into
thyroid storm.

SUPPORTIVE THERAPY
In
Endemic Goiter

SUPPORTIVE THERAPY
In
Endemic Goiter
• The pituitary gland produces thyrotropin or TSH, a
hormone that controls the release of thyroid hormone
from the thyroid gland.
• Its production increases if there is subnormal thyroid
activity, as when insufficient iodine is available for
production of the thyroid hormone.
• Such goiters usually cause no symptoms, except for the
swelling in the neck, which may result in tracheal
compression when excessive.
• Many goiters of this type recede after iodine imbalance
is corrected.

SUPPORTIVE THERAPY
In
Endemic Goiter
• Supplementary iodine, such as SSKI, is prescribed to
suppress the pituitary’s thyroid-stimulating activity.
• When surgery is recommended, the risk for
postoperative complications is minimized by ensuring a
preoperative euthyroid state by treatment with
antithyroid medications and iodide to reduce the size
and vascularity of the goiter.
• Providing children in iodine-poor regions with iodine
compounds can prevent simple or endemic goiter. If the
mean iodine intake is less than 40 fg/day, the thyroid
gland hypertrophies.

SUPPORTIVE THERAPY
In
Nodular Goiter
• Some thyroid glands are nodular because of areas of
hyperplasia.
• No symptoms may arise as a result of this condition, but
not uncommonly these nodules slowly increase in size,
with some descending into the thorax, where they cause
local pressure symptoms.
• Some nodules become malignant, and some are
associated with a hyperthyroid state.
• Thus, the patient with many thyroid nodules may
eventually require surgery.

SUPPORTIVE THERAPY
In
Thyroid Cancer
• Cancer of the thyroid is much less prevalent than other
forms of cancer; however, it accounts for 90% of
endocrine malignancies.
• There are several types of cancer of the thyroid gland;
the type determines the course and prognosis.
• External radiation of the head, neck, or chest in infancy
and childhood increases the risk of thyroid carcinoma.

SUPPORTIVE THERAPY
In
Thyroid Cancer

SUPPORTIVE THERAPY
In
• Lesions that are single, hard, and fixed on palpation or
associated with cervical lymphadenopathy suggest
malignancy.
• Thyroid function tests may be helpful in evaluating
thyroid nodules and masses; however, their results are
rarely conclusive.
• Needle biopsy of the thyroid gland is used as an
outpatient procedure to make a diagnosis of thyroid
cancer, to differentiate cancerous thyroid nodules from
noncancerous nodules, and to stage the cancer if
detected.

SUPPORTIVE THERAPY
In
• A second type of aspiration or biopsy uses a largebore
needle rather than the fine needle used in standard
biopsy; it may be used when the results of the standard
biopsy are inconclusive, or with rapidly growing tumors.
• Additional diagnostic studies include ultrasound, MRI,
CT scans, thyroid scans, radioactive iodine uptake
studies, and thyroid suppression tests.

SUPPORTIVE THERAPY
In
Medical Management
• The treatment of choice for thyroid carcinoma is surgical
removal.
• Total or near-total thyroidectomy is performed when
possible.
• Modified neck dissection or more extensive radical neck
dissection is performed if there is lymph node
involvement.
• Efforts are made to spare parathyroid tissue to reduce
the risk for postoperative hypocalcemia and tetany.
• After surgery, ablation procedures are carried out with
radioactive iodine to eradicate residual thyroid tissue if
the tumor is radiosensitive.

SUPPORTIVE THERAPY
In
Medical Management
• Radioactive iodine also maximizes the chance of
discovering thyroid metastasis at a later date if total-body
scans are carried out.
• After surgery, thyroid hormone is administered in
suppressive doses to lower the levels of TSH to a euthyroid
state.
• If remaining thyroid tissue is inadequate to produce
sufficient thyroid hormone, thyroxine is required
permanently.
• The patient who receives external sources of radiation
therapy is at risk for mucositis, dryness of the mouth,
dysphagia, redness of the skin, anorexia, and fatigue.
• Chemotherapy is infrequently used to treat thyroid cancer.

SUPPORTIVE THERAPY
In
Medical Management
• Postoperatively, the patient is instructed to take
exogenous thyroid hormone to prevent hypothyroidism.
• Later follow-up includes clinical assessment for
recurrence of nodules or masses in the neck and signs
of hoarseness, dysphagia, or dyspnea.
• Total body scans are performed 2 to 4 months after
surgery to detect residual thyroid tissue or metastatic
disease.
• FT4, TSH, serum calcium, and phosphorus levels are
monitored to determine whether the thyroid hormone
supplementation is adequate and to note whether
calcium balance is maintained.

SUPPORTIVE THERAPY
In
Medical Management
• Although local and systemic reactions to radiation may
occur and may include neutropenia or
thrombocytopenia, these complications are rare when
radioactive iodine is used.
• Patients who undergo surgery that is combined with
radioiodine have a higher survival rate than those
undergoing surgery alone.
• Patient teaching emphasizes the importance of taking
prescribed medications and following recommendations
for follow-up monitoring.

SUPPORTIVE THERAPY
In
Nursing Management
• Important preoperative goals are to gain the patient’s
confidence and reduce anxiety.
• Often, the patient’s home life has become tense
because of his or her restlessness, irritability, and
nervousness secondary to hyperthyroidism.
• Efforts are necessary to protect the patient from such
tension and stress to avoid precipitating thyroid storm.
• If the patient reports increased stress when with family
or friends, suggestions are made to limit contact with
them.
• Quiet and relaxing forms of recreation or occupational
therapy may be helpful.

SUPPORTIVE THERAPY
In
Parathyroid Disorders

SUPPORTIVE THERAPY
In
• Parathormone, the protein hormone from the parathyroid
glands, regulates calcium and phosphorus metabolism.
• Increased secretion of parathormone results in
increased calcium absorption from the kidney, intestine,
and bones, thereby raising the blood calcium level.
• Some actions of this hormone are increased by the
presence of vitamin D.
• Parathormone also tends to lower the blood phosphorus
level.
PTH makes the serum calcium increase.

PARATHYROID GLANDS
1. Parathyroid hormone
• Regulates serum calcium
Remember, calcium and phosphorus have an
inverse relationship. When one is elevated, the
other is decreased.

SUPPORTIVE THERAPY
In
• When the product of serum calcium and serum
phosphorus (calcium × phosphorus) rises, calcium
phosphate may precipitate in various organs of the body
and cause tissue calcification.
• The serum level of ionized calcium regulates the output
of parathormone.
• Increased serum calcium results in decreased
parathormone secretion, creating a negative feedback
system.

SUPPORTIVE THERAPY
In
Hyperparathyroidism
• Hyperparathyroidism, which is caused by overproduction
of parathyroid hormone by the parathyroid glands, is
characterized by bone decalcification and the
development of renal calculi containing calcium.
• Primary hyperparathyroidism occurs two to four times
more often in women than in men and is most common
in patients between 60 and 70 years of age.
• The disease is rare in children younger than 15 years,
but the incidence increases tenfold between the ages of
15 and 65 years.
• Half of the patients diagnosed with hyperparathyroidism
do not have symptoms.

SUPPORTIVE THERAPY
In
Hyperparathyroidism
• Secondary hyperparathyroidism, with manifestations
similar to those of primary hyperparathyroidism, occurs
in patients with chronic renal failure and so-called renal
rickets as a result of phosphorus retention, increased
stimulation of the parathyroid glands, and increased
parathyroid hormone secretion.
Hyperparathyroidism is most commonly caused
by a tumor.

SUPPORTIVE THERAPY
In
• Apathy, fatigue, muscle weakness, nausea, vomiting,
constipation, hypertension, and cardiac dysrhythmias
may occur; all are attributable to the increased
concentration of calcium in the blood.
• Psychological manifestations may vary from irritability
and neurosis to psychoses caused by the direct effect of
calcium on the brain and nervous system.
• The formation of stones in one or both kidneys, related
to the increased urinary excretion of calcium and
phosphorus, is one of the important complications of
hyperparathyroidism and occurs in 55% of patients with
primary hyperparathyroidism.

SUPPORTIVE THERAPY
In
• Renal damage results from the precipitation of calcium
phosphate in the renal pelvis and parenchyma, resulting
in renal calculi, obstruction, pyelonephritis, and renal
failure.
• The patient may develop skeletal pain and tenderness,
especially of the back and joints; pain on weight bearing;
pathologic fractures; deformities; and shortening of body
stature.
Remember: calcium acts like a sedative. When
answering test questions about calcium, think muscles
first. Don’t forget the smooth muscles of the body such
as found in the airway or intestines.

SUPPORTIVE THERAPY
In
• Bone loss attributable to hyperparathyroidism increases
the risk for fracture.
• The incidence of peptic ulcer and pancreatitis is
increased with hyperparathyroidism and may be
responsible for many of the gastrointestinal symptoms
that occur.

SUPPORTIVE THERAPY
In
• Primary hyperparathyroidism is diagnosed by persistent
elevation of serum calcium levels and an elevated level
of parathormone.
• Radioimmunoassays for parathormone are sensitive and
differentiate primary hyperparathyroidism from other
causes of hypercalcemia in more than 90% of patients
with elevated serum calcium levels.
• An elevated serum calcium level alone is a nonspecific
finding because serum levels may be altered by diet,
medications, and renal and bone changes.
• Bone changes may be detected on x-ray or bone scans
in advanced disease.

SUPPORTIVE THERAPY
In
• The double antibody parathyroid hormone test is used to
distinguish between primary hyperparathyroidism and
malignancy as a cause of hypercalcemia.
• Ultrasound, MRI, thallium scan, and fine-needle biopsy
have been used to evaluate the function of the
parathyroids and to localize parathyroid cysts,
adenomas, or hyperplasia.

SUPPORTIVE THERAPY
In
Hypercalcemic Crisis
• Serum calcium levels higher than 15 mg/dL (3.7 mmol/L)
result in neurologic, cardiovascular, and renal symptoms
that can be life-threatening.
• Treatment includes rehydration with large volumes of
intravenous fluids, diuretic agents to promote renal
excretion of excess calcium, and phosphate therapy to
correct hypophosphatemia and decrease serum calcium
levels by promoting calcium deposit in bone and
reducing the gastrointestinal absorption of calcium.
• Cytotoxic agents (mithramycin), calcitonin, and dialysis
may be used in emergency situations to decrease serum
calcium levels quickly.

SUPPORTIVE THERAPY
In
• A combination of calcitonin and corticosteroids has been
administered in emergencies to reduce the serum
calcium level by increasing calcium deposition in bone.
• Other agents that may be administered to decrease
serum calcium levels include bisphosphonates (eg,
etidronate [Didronel], pamidronate).
• The patient requires expert assessment and care to
minimize complications and reverse the life-threatening
hypercalcemia.
• Medications are administered with care, and attention is
given to fluid balance to promote return of normal fluid
and electrolyte balance.

SUPPORTIVE THERAPY
In
• Supportive measures are necessary for the patient and
family.situations to decrease serum calcium levels
quickly.

SUPPORTIVE THERAPY
In
Medical Management
• The insidious onset and chronic nature of
hyperparathyroidism and its diverse and commonly vague
symptoms may result in depression and frustration.
• The family may have considered the patient’s illness to be
psychosomatic.
• An awareness of the course of the disorder and an
understanding approach by the nurse may help the patient
and family to deal with their reactions and feelings.
• The recommended treatment of primary
hyperparathyroidism is the surgical removal of abnormal
parathyroid tissue.

SUPPORTIVE THERAPY
In
Medical Management
• In some patients without symptoms and with only mildly
elevated serum calcium levels and normal renal
function, surgery may be delayed and the patient
followed closely for worsening of hypercalcemia, bone
deterioration, renal impairment, or the development of
kidney stones.

SUPPORTIVE THERAPY
In
Medical Management
HYDRATION THERAPY
• Because kidney involvement is possible, patients with
hyperparathyroidism are at risk for renal calculi.
• Fluid intake of 2,000 mL or more is encouraged to help
prevent calculus formation.
• Cranberry juice is suggested because it may lower the
urinary pH. It can be added to juices and ginger ale for
variety.
• The patient is instructed to report other manifestations of
renal calculi, such as abdominal pain and hematuria.

SUPPORTIVE THERAPY
In
Medical Management
HYDRATION THERAPY
• Thiazide diuretics are avoided because they decrease
the renal excretion of calcium and further elevate serum
calcium levels.
• Because of the risk of hypercalcemic crisis, the patient is
instructed to avoid dehydration and to seek immediate
health care if conditions that commonly produce
dehydration (eg, vomiting, diarrhea) occur.

SUPPORTIVE THERAPY
In
Medical Management
MOBILITY
• Mobility of the patient, with walking or use of a rocking
chair for those with limited mobility, is encouraged as
much as possible because bones subjected to normal
stress give up less calcium.
• Bed rest increases calcium excretion and the risk for
renal calculi.
• Oral phosphates lower the serum calcium level in some
patients.
• Long term use is not recommended because of the risk
for ectopic calcium phosphate deposits in soft tissues.

SUPPORTIVE THERAPY
In
Medical Management
DIET AND MEDICATIONS
• Nutritional needs are met, but the patient is advised to
avoid a diet with restricted or excess calcium.
• If the patient has a coexisting peptic ulcer, prescribed
antacids and protein feedings are necessary.
• Because anorexia is common, efforts are made to
improve the appetite.
• Prune juice, stool softeners, and physical activity, along
with increased fluid intake, help to offset constipation,
which is common postoperatively.

SUPPORTIVE THERAPY
In
Nursing Management
• Although not all parathyroid tissue is removed during
surgery in an effort to control the calcium–phosphorus
balance, the nurse closely monitors the patient to detect
symptoms of tetany (which may be an early
postoperative complication).
• The nurse reminds the patient and family about the
importance of follow-up to ensure return of serum
calcium levels to normal.

SUPPORTIVE THERAPY
In
Hypoparathyroidism
• The most common cause of hypoparathyroidism is
inadequate secretion of parathyroid hormone after
interruption of the blood supply or surgical removal of
parathyroid gland tissue during thyroidectomy,
parathyroidectomy, or radical neck dissection.
• Atrophy of the parathyroid glands of unknown cause is a
less common cause of hypoparathyroidism.

SUPPORTIVE THERAPY
In
Pathophysiology
• Symptoms of hypoparathyroidism are caused by a
deficiency of parathormone that results in elevated blood
phosphate (hyperphosphatemia) and decreased blood
calcium (hypocalcemia) levels.
• In the absence of parathormone, there is decreased
intestinal absorption of dietary calcium and decreased
resorption of calcium from bone and through the renal
tubules.
• Decreased renal excretion of phosphate causes
hypophosphaturia, and low serum calcium levels result
in hypocalciuria.

SUPPORTIVE THERAPY
In
• Hypocalcemia causes irritability of the neuromuscular
system and contributes to the chief symptom of
hypoparathyroidism—tetany.
• Tetany is a general muscle hypertonia, with tremor and
spasmodic or uncoordinated contractions occurring with
or without efforts to make voluntary movements.
• Symptoms of latent tetany are numbness, tingling, and
cramps in the extremities, and the patient complains of
stiffness in the hands and feet.
• In overt tetany, the signs include bronchospasm,
laryngeal spasm, carpopedal spasm, dysphagia,
photophobia, cardiac dysrhythmias and seizures.

SUPPORTIVE THERAPY
In
• Other symptoms include anxiety, irritability, depression,
and even delirium. ECG changes and hypotension also
may occur.

SUPPORTIVE THERAPY
In
• A positive Trousseau’s sign or a positive Chvostek’s
sign suggests latent tetany.
• Trousseau’s sign is positive when carpopedal spasm is
induced by occluding the blood flow to the arm for 3
minutes with a blood pressure cuff.
• Chvostek’s sign is positive when a sharp tapping over
the facial nerve just in front of the parotid gland and
anterior to the ear causes spasm or twitching of the
mouth, nose, and eye.
• The diagnosis of hypoparathyroidism often is difficult
because of the vague symptoms, such as aches and
pains.

SUPPORTIVE THERAPY
In
• Tetany develops at serum calcium levels of 5 to 6 mg/dL
(1.2 to 1.5 mmol/L) or lower.
• Serum phosphate levels are increased, and x-rays of
bone show increased density.
• Calcification is detected on x-rays of the subcutaneous
or paraspinal basal ganglia of the brain.
Chvostek’s sign is unilateral contraction of facial
muscles when the cheek is tapped. Trousseau’s sign is
a hand tremor in response to the pumping up of a
blood pressure cuff on the same arm.

SUPPORTIVE THERAPY
In
Medical Management
• The goal of therapy is to raise the serum calcium level to
9 to 10 mg/dL (2.2 to 2.5 mmol/L) and to eliminate the
symptoms of hypoparathyroidism and hypocalcemia.
• When hypocalcemia and tetany occur after a
thyroidectomy, the immediate treatment is to administer
calcium gluconate intravenously.
• If this does not decrease neuromuscular irritability and
seizure activity immediately, sedative agents such as
pentobarbital may be administered.
• Parenteral parathormone can be administered to treat
acute hypoparathyroidism with tetany.

SUPPORTIVE THERAPY
In
Medical Management
• The high incidence of allergic reactions to injections of
parathormone, however, limits its use to acute episodes
of hypocalcemia.
• The patient receiving parathormone is monitored closely
for allergic reactions and changes in serum calcium
levels.
• Because of neuromuscular irritability, the patient with
hypocalcemia and tetany requires an environment that is
free of noise, drafts, bright lights, or sudden movement.
• Tracheostomy or mechanical ventilation may become
necessary, along with bronchodilating medications, if the
patient develops respiratory distress.

SUPPORTIVE THERAPY
In
Medical Management
• A diet high in calcium and low in phosphorus is prescribed.
• Although milk, milk products, and egg yolk are high in
calcium, they are restricted because they also contain high
levels of phosphorus.
• Spinach also is avoided because it contains oxalate, which
would form insoluble calcium substances.
• Oral tablets of calcium salts, such as calcium gluconate,
may be used to supplement the diet.
• Aluminum hydroxide gel or aluminum carbonate (Gelusil,
Amphojel) also is administered after meals to bind
phosphate and promote its excretion through the
gastrointestinal tract.

SUPPORTIVE THERAPY
In
Medical Management
• Variable dosages of a vitamin D preparation—
dihydrotachysterol (AT 10 or Hytakerol), ergocalciferol
(vitamin D), cholecalciferol (vitamin D)—are usually
required and enhance calcium absorption from the
gastrointestinal tract.

SUPPORTIVE THERAPY
In
Nursing Management
• Care of postoperative patients having thyroidectomy,
parathyroidectomy, and radical neck dissection is directed
toward detecting early signs of hypocalcemia and
anticipating signs of tetany, seizures, and respiratory
difficulties.
• Calcium gluconate is kept at the bedside, with equipment
necessary for intravenous administration.
• If the patient has a cardiac disorder, is subject to
dysrhythmias, or is receiving digitalis, calcium gluconate is
administered slowly and cautiously.
• Calcium and digitalis increase systolic contraction and also
potentiate each other; this may produce potentially fatal
dysrhythmias.

SUPPORTIVE THERAPY
In
Nursing Management
• Consequently, the cardiac patient requires continuous
cardiac monitoring and careful assessment.
• An important aspect of nursing care is teaching about
medications and diet therapy.
• The patient needs to know the reason for high calcium
and low phosphate intake and the symptoms of
hypocalcemia and hypercalcemia; he or she should
know to contact the physician immediately if these
symptoms occur.

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In
Adrenal Disorders
• There are two adrenal glands in the human, each
attached to the upper portion of a kidney.
• Each adrenal gland is, in reality, two endocrine glands
with separate, independent functions.
• The adrenal medulla at the center of the gland secretes
catecholamines, and the outer portion of the gland, the
adrenal cortex, secretes steroid hormones.
• The secretion of hormones from the adrenal cortex is
regulated by the hypothalamicpituitary- adrenal axis.
• The hypothalamus secretes corticotropinreleasing
hormone (CRH), which in turn stimulates the pituitary
gland to secrete ACTH.

SUPPORTIVE THERAPY
In
Adrenal Disorders
• ACTH then stimulates the adrenal cortex to secrete
glucocorticoid hormone (cortisol).
• Increased levels of the adrenal hormone then inhibit the
production or secretion of CRH and ACTH.
• This system is an example of a negative feedback
mechanism.

SUPPORTIVE THERAPY
In
Adrenal Function
ADRENAL MEDULLA
• The adrenal medulla functions as part of the autonomic
nervous system.
• Stimulation of preganglionic sympathetic nerve fibers,
which travel directly to the cells of the adrenal medulla,
causes release of the catecholamine hormones
epinephrine and norepinephrine.
• About 90% of the secretion of the human adrenal
medulla is epinephrine.
• Catecholamines regulate metabolic pathways to
promote catabolism of stored fuels to meet caloric needs
from endogenous sources.

SUPPORTIVE THERAPY
In
Adrenal Function
ADRENAL MEDULLA
• The major effects of epinephrine release are to prepare
to meet a challenge (fight-or-flight response).
• Secretion of epinephrine causes decreased blood flow
to tissues that are not needed in emergency situations,
such as the gastrointestinal tract, and causes increased
blood flow to tissues that are important for effective fight
or flight, such as cardiac and skeletal muscle.
• Catecholamines also induce the release of free fatty
acids, increase the basal metabolic rate, and elevate the
blood glucose level.

SUPPORTIVE THERAPY
In
Adrenal Function
ADRENAL CORTEX
• A functioning adrenal cortex is necessary for life;
adrenocortical secretions make it possible for the body
to adapt to stress of all kinds.
• The three types of steroid hormones produced by the
adrenal cortex are glucocorticoids, the prototype of
which is hydrocortisone; mineralocorticoids, mainly
aldosterone; and sex hormones, mainly androgens
(male sex hormones).
• Without the adrenal cortex, severe stress would cause
peripheral circulatory failure, circulatory shock, and
prostration.

SUPPORTIVE THERAPY
In
Adrenal Function
ADRENAL CORTEX
• Survival in the absence of a functioning adrenal cortex is
possible only with nutritional, electrolyte, and fluid
replacement and appropriate replacement with
exogenous adrenocortical hormones.
Many heart attacks occur during the early morning
hours when people are coming out of REM sleep, as
this is a very stressful time for the body.
The steroids produced by the adrenal cortex (cortical
steroids) are made from cholesterol.
CHOLESTEROL IS GOOD FOR YOU!

SUPPORTIVE THERAPY
In
Adrenal Function
GLUCOCORTICOIDS
• The glucocorticoids are so named because they have an
important influence on glucose metabolism: increased
hydrocortisone secretion results in elevated blood
glucose levels.
• Glucocorticoids are secreted from the adrenal cortex in
response to the release of ACTH from the anterior lobe
of the pituitary gland.
• The presence of glucocorticoids in the blood inhibits the
release of corticotropin-releasing factor from the
hypothalamus and also inhibits ACTH secretion from the
pituitary.

SUPPORTIVE THERAPY
In
Adrenal Function
GLUCOCORTICOIDS
• The resultant decrease in ACTH secretion causes
diminished release of glucocorticoids from the adrenal
cortex.
• Glucocorticoids are administered frequently to inhibit the
inflammatory response to tissue injury and suppress
allergic manifestations.
• Their side effects include the development of diabetes
mellitus, osteoporosis, peptic ulcer, increased protein
breakdown resulting in muscle wasting and poor wound
healing, and redistribution of body fat.

SUPPORTIVE THERAPY
In
Adrenal Function
GLUCOCORTICOIDS
• Large amounts of exogenously administered
glucocorticoids in the blood inhibit the release of ACTH
and endogenous glucocorticoids.
• Because of this, the adrenal cortex can atrophy.
• If exogenous glucocorticoid administration is
discontinued suddenly, adrenal insufficiency results
because of the inability of the atrophied cortex to
respond adequately.

SUPPORTIVE THERAPY
In
Adrenal Function
MINERALOCORTICOIDS
• Mineralocorticoids exert their major effects on electrolyte
metabolism.
• They act principally on the renal tubular and
gastrointestinal epithelium to cause increased sodium
ion absorption in exchange for excretion of potassium or
hydrogen ions.
• ACTH only minimally influences aldosterone secretion.
• It is primarily secreted in response to the presence of
angiotensin II in the bloodstream.
• Angiotensin II is a substance that elevates the blood
pressure by constricting arterioles.

SUPPORTIVE THERAPY
In
Adrenal Function
MINERALOCORTICOIDS
• Its concentration is increased when renin is released
from the kidney in response to decreased perfusion
pressure.
• The resultant increased aldosterone levels promote
sodium reabsorption by the kidney and the
gastrointestinal tract, which tends to restore blood
pressure to normal.
• The release of aldosterone is also increased by
hyperkalemia.
• Aldosterone is the primary hormone for the long-term
regulation of sodium balance.

SUPPORTIVE THERAPY
In
Adrenal Function
ADRENAL SEX HORMONES
• Androgens, the third major type of steroid hormones
produced by the adrenal cortex, exert effects similar to
those of male sex hormones.
• The adrenal gland may also secrete small amounts of
some estrogens, or female sex hormones.
• ACTH controls the secretion of adrenal androgens.
When secreted in normal amounts, the adrenal
androgens probably have little effect, but when secreted
in excess, in certain inborn enzyme deficiencies,
masculinization may result.
• This is termed the ADRENOGENITAL SYNDROME.

ADRENAL CORTEX
1. Mineralocorticosteroids, mainly aldosterone
• Increases sodium absorption and potassium loss by
the kidneys.
2. Glucocorticoids, mainly cortisol
• Affects metabolism of all nutrients; regulates blood
glucose levels, affects growth, has anti-inflammatory
action, and decreases effects of stress

ADRENAL CORTEX
3. Adrenal androgens, dehydroepiandrosterone DHEA
and androstenedione
• Have minimal intrinsic androgenic activity; they are
converted to testosterone and dihydrotestosterone in
the periphery
Synthetic androgens (sex hormones) are referred
to as anabolic steroids.

ADRENAL MEDULLA
1. Epinephrine
2. Norepinephrine
• Serve as neurotransmitters for the sympathetic
nervous system

SUPPORTIVE THERAPY
In
Pheochromocytoma
• Pheochromocytoma is a tumor that is usually benign
and originates from the chromaffin cells of the adrenal
medulla.
• Pheochromocytoma may occur at any age, but its peak
incidence is between ages 40 and 50 years.
• It affects men and women equally.
• Because of the high incidence of pheochromocytoma in
family members, the patient’s family members should be
alerted and screened for this tumor.

SUPPORTIVE THERAPY
In
Pheochromocytoma
• Pheochromocytoma is the cause of high blood pressure
in 0.2% of patients with new onset of hypertension.
• Pheochromocytoma may occur in the familial form as
part of multiple endocrine neoplasia type 2; therefore, it
should be considered a possibility in patients with
medullary thyroid carcinoma and parathyroid
hyperplasia or tumor.

SUPPORTIVE THERAPY
In
• The nature and severity of symptoms of functioning
tumors of the adrenal medulla depend on the relative
proportions of epinephrine and norepinephrine
secretion.
• The typical triad of symptoms comprises headache,
diaphoresis, and palpitations.
• Hypertension and other cardiovascular disturbances are
common. The hypertension may be intermittent or
persistent.
• Other symptoms may include tremor, headache,
flushing, and anxiety.

SUPPORTIVE THERAPY
In
• Hyperglycemia may result from conversion of liver and
muscle glycogen to glucose by epinephrine secretion;
insulin may be required to maintain normal blood
glucose levels.
• The clinical picture in the paroxysmal form of
pheochromocytoma is usually characterized by acute,
unpredictable attacks lasting seconds or several hours.
During these attacks, the patient is extremely anxious,
tremulous, and weak.
• The patient may experience headache, vertigo, blurring
of vision, tinnitus, air hunger, and dyspnea.

SUPPORTIVE THERAPY
In
• Other symptoms include polyuria, nausea, vomiting,
diarrhea, abdominal pain, and a feeling of impending
doom.
• Palpitations and tachycardia are common.
• Blood pressures exceeding 250/150 mm Hg have been
recorded. Such blood pressure elevations are life-
threatening and may cause severe complications, such
as cardiac dysrhythmias, dissecting aneurysm, stroke,
and acute renal failure.
• Postural hypotension occurs in 70% of patients with
untreated pheochromocytoma.

SUPPORTIVE THERAPY
In
• Pheochromocytoma is suspected if signs of sympathetic
nervous system overactivity occur in association with
marked elevation of blood pressure.
• These signs can be associated with the ―five Hs‖:
hypertension, headache, hyperhidrosis,
hypermetabolism, and hyperglycemia.
• Measurements of urine and plasma levels of
catecholamines are the most direct and conclusive tests
for overactivity of the adrenal medulla.
• A 24-hour specimen of urine is collected for determining
free catecholamines.

SUPPORTIVE THERAPY
In
• A number of medications and foods (eg, coffee, tea,
bananas, chocolate, vanilla, aspirin) may alter the results
of these tests; therefore, careful instructions to avoid
restricted items must be given to the patient.
• Total plasma catecholamine (epinephrine and
norepinephrine) concentration is measured with the patient
supine and at rest for 30 minutes.
• Factors that may elevate catecholamine levels must be
controlled to obtain valid results; these factors include
consumption of coffee or tea, use of tobacco, emotional
and physical stress, and use of many prescription and
over-the-counter medications (eg, amphetamines, nose
drops or sprays, decongestant agents, and
bronchodilators).

SUPPORTIVE THERAPY
In
• Normal plasma values of epinephrine are 100 pg/mL
(590 pmol/L); normal values of norepinephrine are
generally less than 100 to 550 pg/mL (590 to 3,240
pmol/L).
• Values of epinephrine greater than 400 pg/mL (2,180
pmol/L) or norepinephrine values greater than 2,000
pg/mL (11,800 pmol/L) are considered diagnostic of
pheochromocytoma.

SUPPORTIVE THERAPY
In
• Imaging studies, such as CT scans, MRI, and
ultrasound, may also be carried out to localize the
pheochromocytoma and to determine whether more
than one tumor is present.
• Use of 131I-metaiodobenzylguanidine (MIBG)
scintigraphy may be required to determine the location
of the pheochromocytoma and to detect metastatic sites
outside the adrenal gland.
• MIBG scintigraphy is a noninvasive, safe procedure that
has increased the accuracy of diagnosis of adrenal
tumors.

SUPPORTIVE THERAPY
In
Medical Management
• The patient may be moved to the intensive care unit for
close monitoring of ECG changes and careful
administration of alphaadrenergic blocking agents (eg,
phentolamine [Regitine]) or smooth muscle relaxants (eg,
sodium nitroprusside [Nipride]) to lower the blood pressure
quickly.
• Phenoxybenzamine (Dibenzyline), a long-acting alpha-
blocker, may be used when the blood pressure is stable to
prepare the patient for surgery.
• Beta-adrenergic blocking agents, such as propranolol
(Inderal), may be used in patients with cardiac
dysrhythmias or those not responsive to alpha-blockers.

SUPPORTIVE THERAPY
In
Medical Management
• Alphaadrenergic and beta-adrenergic blocking agents
must be used with caution because patients with
pheochromocytoma may have increased sensitivity to
them.
• Still other medications that may be used preoperatively
are catecholamine synthesis inhibitors, such as alpha-
methyl-p-tyrosine (metyrosine).
• These are occasionally used when adrenergic blocking
agents do not reduce the effects of catecholamines.

SUPPORTIVE THERAPY
In
Medical Management
SURGICAL MANAGEMENT
• The definitive treatment of pheochromocytoma is
surgical removal of the tumor, usually with
ADRENALECTOMY.
• Bilateral adrenalectomy may be necessary if tumors are
present in both adrenal glands.
• Phentolamine or phenoxybenzamine (Dibenzyline) may
be used safely without causing undue hypotension.
• Other medications (metyrosine [Demser] and prazosin
[Minipress]) have been used to treat
pheochromocytoma.

SUPPORTIVE THERAPY
In
Medical Management
SURGICAL MANAGEMENT
• The patient needs to be well hydrated before, during,
and after surgery to prevent hypotension.
• Corticosteroid replacement is required if bilateral
adrenalectomy has been necessary.

SUPPORTIVE THERAPY
In
Nursing Management
• The patient who has undergone surgery to treat
pheochromocytoma has experienced a stressful
preoperative and postoperative course and may remain
fearful of repeated attacks.
• The patient is monitored for several days in the intensive
care unit with special attention given to ECG changes,
arterial pressures, fluid and electrolyte balance, and
blood glucose levels.
• Several intravenous lines are inserted for administration
of fluids and medications.

SUPPORTIVE THERAPY
In
Adrenocortical Deficiencies
• ADDISON’S DISEASE, results when adrenal cortex
function is inadequate to meet the patient’s need for
cortical hormones.
• Autoimmune or idiopathic atrophy of the adrenal glands
is responsible for 80% of cases.
• Other causes include surgical removal of both adrenal
glands or infection of the adrenal glands.
• Tuberculosis and histoplasmosis are the most common
infections that destroy adrenal gland tissue.
• Inadequate secretion of ACTH from the pituitary gland
also results in adrenal insufficiency because of
decreased stimulation of the adrenal cortex.

SUPPORTIVE THERAPY
In
Adrenocortical Deficiencies
• Therapeutic use of corticosteroids is the most common
cause of adrenocortical insufficiency.
• Treatment with daily administration of corticosteroids for
2 to 4 weeks may suppress function of the adrenal
cortex; therefore, adrenal insufficiency should be
considered in any patient who has been treated with
corticosteroids.
The most common cause of Addison’s disease is
an autoimmune response. The adrenal cortex
loses about 90% of its function before any clinical
manifestations appear.

SUPPORTIVE THERAPY
In
• Addison’s disease is characterized by muscle weakness,
anorexia, gastrointestinal symptoms, fatigue,
emaciation, dark pigmentation of the skin, knuckles,
knees, elbows, and mucous membranes, hypotension,
and low blood glucose levels, low serum sodium levels,
and high serum potassium levels.
• Mental status changes such as depression, emotional
lability, apathy, and confusion are present in 60% to 80%
of patients.
• In severe cases, the disturbance of sodium and
potassium metabolism may be marked by depletion of
sodium and water and severe, chronic dehydration.

SUPPORTIVE THERAPY
In
• With disease progression and acute hypotension, the
patient develops ADDISONIAN CRISIS, which is
characterized by cyanosis and the classic signs of
circulatory shock: pallor, apprehension, rapid and weak
pulse, rapid respirations, and low blood pressure.
• In addition, the patient may complain of headache,
nausea, abdominal pain, and diarrhea and show signs of
confusion and restlessness.
• Even slight overexertion, exposure to cold, acute
infections, or a decrease in salt intake may lead to
circulatory collapse, shock, and death if untreated.

SUPPORTIVE THERAPY
In
• Laboratory findings include decreased blood glucose
(hypoglycemia) and sodium (hyponatremia) levels, an
increased serum potassium (hyperkalemia) level, and an
increased white blood cell count (leukocytosis).
• The diagnosis is confirmed by low levels of
adrenocortical hormones in the blood or urine and
decreased serum cortisol levels.
• If the adrenal cortex is destroyed, baseline values are
low, and ACTH administration fails to cause the normal
rise in plasma cortisol and urinary 17-
hydroxycorticosteroids.

SUPPORTIVE THERAPY
In
Medical Management
• Immediate treatment is directed toward combating
circulatory shock: restoring blood circulation,
administering fluids and corticosteroids, monitoring vital
signs, and placing the patient in a recumbent position
with the legs elevated.
• Hydrocortisone (Solu-Cortef) is administered
intravenously, followed with 5% dextrose in normal
saline.
• Vasopressor amines may be required if hypotension
persists.
• Antibiotics may be administered if infection has
precipitated adrenal crisis in a patient with chronic
adrenal insufficiency.

SUPPORTIVE THERAPY
In
Medical Management
• Additionally, the patient is assessed closely to identify
other factors, stressors, or illnesses that led to the acute
episode.
• The patient will require additional supplementary therapy
with glucocorticoids during stressful procedures or
significant illnesses to prevent addisonian crisis.
• Additionally, the patient may need to supplement dietary
intake with added salt during times of gastrointestinal
losses of fluids through vomiting and diarrhea.
For clients who take steroids, teach them to never
stop taking the steroid suddenly, as this could
result in an addisonian crisis, shock, and death.

SUPPORTIVE THERAPY
In
Nursing Management
ASSESSING THE PATIENT
• The health history and examination focus on the presence
of symptoms of fluid imbalance and on the patient’s level of
stress.
• To detect inadequate fluid volume, the nurse monitors the
blood pressure and pulse rate as the patient moves from a
lying to a standing position.
• The nurse assesses the skin color and turgor for changes
related to chronic adrenal insufficiency and hypovolemia.
• Other key assessments include checking for weight
changes, muscle weakness, and fatigue and investigating
any illness or stress that may have precipitated the acute
crisis.

SUPPORTIVE THERAPY
In
Nursing Management
MONITORING AND MANAGING ADDISONIAN CRISIS
• The patient at risk is monitored for signs and symptoms
indicative of addisonian crisis.
• These symptoms are often the manifestations of shock:
hypotension; rapid, weak pulse; rapid respiratory rate;
pallor; and extreme weakness.
• The patient with addisonian crisis is at risk for circulatory
collapse and shock; therefore, physical and
psychological stressors must be avoided.
• These include exposure to cold, overexertion, infection,
and emotional distress.

SUPPORTIVE THERAPY
In
Nursing Management
• The patient with addisonian crisis requires immediate
treatment with intravenous administration of fluid,
glucose, and electrolytes, especially sodium;
replacement of missing steroid hormones; and
vasopressors.
• During acute addisonian crisis, the patient must avoid
exertion; therefore, the nurse anticipates the patient’s
needs and takes measures to meet them.

SUPPORTIVE THERAPY
In
Nursing Management
• The patient with addisonian crisis requires immediate
treatment with intravenous administration of fluid,
glucose, and electrolytes, especially sodium;
replacement of missing steroid hormones; and
vasopressors.
• During acute addisonian crisis, the patient must avoid
exertion; therefore, the nurse anticipates the patient’s
needs and takes measures to meet them.
• Careful monitoring of symptoms, vital signs, weight, and
fluid and electrolyte status is essential to monitor the
patient’s progress and return to a precrisis state.

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