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Chapter 44
Pituitary and Adrenal
Disorders
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1
Learning Objectives
• Identify data to be collected for the nursing assessment
of adrenal and pituitary function.
• Describe the tests and procedures used to diagnose disorders of the
adrenal and pituitary glands.
• Describe the pathophysiology and medical treatment of
adrenocortical insufficiency, excess adrenocortical hormones,
hypopituitarism, diabetes insipidus, and pituitary tumors.
• Assist in developing nursing care plans for patients with
selected disorders of the adrenal and pituitary glands.
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Hormone Functions and Regulation
• Released in response to body’s needs
• Responsible for reproduction, fluid and
electrolyte balance, host defenses, responses
to stress and injury, energy metabolism, and
growth and development
• Endocrine system: maintain homeostasis
• Maintenance of physiologic stability despite
constant changes in the environment
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Hormone Functions and Regulation
• Feedback mechanisms
• Controls regulation of endocrine activity by either
stimulating or inhibiting hormone synthesis and
secretion
• Triggered by blood levels of specific substances
• May be positive or negative
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The Pituitary Gland
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Anatomy and Physiology
• Weighs approximately 0.6 g; located in the
sella turcica, a small indentation in the
sphenoid bone at the base of the brain
• Connected to the hypothalamus by the
infundibular (hypophyseal) stalk
• Small and oval; diameter of about 1 cm
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Figure 44-1
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Anatomy and Physiology
• Anterior lobe
• Larger of the two lobes: accounts for 70% to 80% of the
gland’s weight
• Called the adenohypophysis
• Secretes
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Growth hormone (GH), or somatotropic hormone
Adrenocorticotropic hormone (ACTH)
Thyroid-stimulating hormone or thyrotropic hormone
Follicle-stimulating hormone
Luteinizing hormone
Prolactin, or lactogenic hormone
Melanocyte-stimulating hormone
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Anatomy and Physiology
• Posterior lobe
• The smaller lobe
• Also called the neurohypophysis
• Secretes
• Antidiuretic hormone (ADH), or vasopressin
• Oxytocin
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Health History
• Present illness
• Slowed or accelerated growth, visual disturbances, headache,
and changes in urine output, appearance, skin, and secondary
sex characteristics
• Past medical history
• Brain tumors, pituitary surgery, head trauma, central nervous
system infection, vascular disorders, chronic renal failure,
hypothyroidism, and disease of the pancreas, liver, or bone
• Family history of diabetes insipidus
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Health History
• Review of systems
• Fatigue, weakness, restlessness, or agitation
• Skin moisture and changes in body hair distribution
• Significant sensory changes such as blurred vision
and diplopia (double vision)
• Changes in the breasts
• Chest pain, constipation, polyuria, changes in
genitalia, sexual dysfunction, joint pain, abnormal
sensations, edema, seizures, and intolerance of
heat or cold
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Health History
• Functional assessment
• Determine whether the patient has had sleep
disturbances
• Usual diet; note the effects of symptoms on the
person’s self-concept and usual activities
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Physical Assessment
• Vital signs, height, and weight
• Skin for moisture and edema
• Inspect head and face for thickened lips, broad nose, and
prominent forehead and jaw; test visual acuity
• Inspect the breasts for enlargement in men, atrophy in women,
and nipple discharge
• Inspect and palpate the extremities for edema. Perform joint range
of motion, noting any limitations or crepitus
• Test reflexes for slowness of response
• Male genitalia loss of hair; palpate for testicular atrophy
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Age-Related Changes
• In healthy older adults, pituitary function
remains adequate
• Increased ADH secretion impairs ability to
concentrate urine, increasing risk of
dehydration
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Diagnostic Tests and Procedures
• Radiographic studies
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Conventional radiographs
Computed tomographic (CT) scans
MRI
Cerebral angiography
• Laboratory studies
• Radioimmunoassay
• Enzyme-linked immunosorbent assay (ELISA)
• Hormone reserve activity also can be measured using a
number of “suppression” or “stimulation” tests
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Pituitary Disease
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Figure 44-2
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Disorders of the Pituitary Gland
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Hyperpituitarism
• Etiology
• Pathologic state caused by excess production of
one or more of the anterior pituitary hormones
• Common factor is presence of a pituitary adenoma
• Growth hormone and prolactin often in excess
• Overproduction leads to gigantism or acromegaly
• Overproduction of prolactin causes prolactemia
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Figure 44-3
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Figure 44-4
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Hyperpituitarism
• Medical diagnosis
• Radiographic studies
• CT scans using a water-soluble dye
• MRI
• Laboratory studies
• Anterior pituitary hormone levels
• Dexamethasone suppression tests
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Hyperpituitarism
• Medical treatment
• Drug therapy
• Somatostatin analogs, dopamine agonists, GH receptor
antagonists, and octreotide (Sandostatin)
• Radiation
• Surgical management
• Hypophysectomy: surgical removal of the adenoma or of
the pituitary
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Figure 44-5
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Hyperpituitarism
• Assessment
• Gigantism/acromegaly: energy level, height/weight, vital signs,
contours of the face and skull, visual acuity, speech, voice
quality, abdominal distention
• If surgery, determine what patient knows and expects
• Interventions
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Disturbed Body Image
Activity Intolerance
Chronic Pain
Ineffective Therapeutic Regimen Management
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Hyperpituitarism
• Postoperative nursing care
• Assessment
• Neurologic status and vision must be monitored closely
with particular attention to level of consciousness, pupil
size and equality, and vital signs
• Intake and output
• Inspect nasal packing
• Signs and symptoms of infection
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Hyperpituitarism
• Postoperative nursing care
• Interventions
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Anxiety
Impaired Sensory Perception
Acute Pain and Impaired Oral Mucous Membrane
Risk for Injury
Excess Fluid Volume or Deficient Fluid Volume
Risk for Infection
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Etiology and Pathophysiology
• Dwarfism
• Inadequate secretion of growth hormone during
preadolescence
• Attainment of a maximum height 40% below normal
• Causes hereditary or related to damage to the anterior portion
of the pituitary gland
• Panhypopituitarism
• Growth has been completed and some pathologic process
impairs the function of the pituitary
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Hypopituitarism
• Signs and symptoms
• Depends on the stage of life which hormones are
deficient
• Dwarfism
• Occurs early; person as short as 36 inches but with
proportional physical characteristics
• Often have delayed or absent sexual maturation
• Accelerated pattern of aging, thus shorter life span
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Hypopituitarism
• Signs and symptoms
• Panhypopituitarism
• Simmonds’ cachexia
• Muscle and organ wasting and disruptions of both digestion
and metabolism
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Absence of ACTH affects ability to cope with stress
Thyroid-stimulating hormone is depleted
Decreased pigmentation of the skin
Gonads may become atrophied
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Hypopituitarism
• Medical diagnosis
• Health history, physical examination, diagnostic
tests
• Conventional radiographs and CT scans
• Cerebral angiography
• Serum levels of pituitary hormones
• Medical and surgical treatment
• Deficient hormones are replaced as needed
• If caused by tumor, surgery, or radiation
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Hypopituitarism
• Assessment
• Sense of well-being, energy level, appetite
• Changes in skin texture, body temperature, hair,
and libido
• Determine whether there has been difficulty carrying
out usual activities
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Hypopituitarism
• Interventions
• Education important: disturbances in body image,
sexual function, nutritional status, and fluid balance
can be improved if patient follows the prescribed
therapy
• Acknowledge patient’s feelings and encourage
expression of concerns; refer to a mental health
counselor if patient has difficulty dealing with the
effects of the disease
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Diabetes Insipidus (DI)
• Etiology
• Excessive output of dilute urine
• Nephrogenic DI
• Inherited defect: renal tubules do not respond to ADH, resulting in
inadequate water reabsorption
• Neurogenic DI
• A defect in either the production or secretion of ADH
• Dipsogenic DI
• A disorder of thirst stimulation
• When patient ingests water, serum osmolality decreases, which
causes reduced vasopressin secretion
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Diabetes Insipidus
• Pathophysiology
• Antidiuretic hormone deficiency or inability of kidneys to
respond to ADH results in the excretion of large volumes of
very dilute urine
• Signs and symptoms
• Massive diuresis, dehydration, and thirst
• Malaise, lethargy, and irritability
• Medical diagnosis
• Health history, physical examination, and laboratory findings
• 24-hour urine output of greater than 4 L of fluid
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Diabetes Insipidus
• Medical treatment
• Intravenous fluid volume replacement and
vasopressors often required to maintain adequate
blood pressure
• Neurogenic DI
• DDAVP (desmopressin acetate)
• Sodium intake restricted and thiazide diuretics prescribed
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Diabetes Insipidus
• Assessment
• Thirst, change in urine appearance or volume, dizziness,
weakness, fainting, and palpitations
• Hydration, including skin turgor, moisture of mucous
membranes, pulse rate and quality, blood pressure, and
mental status
• Intake and output, daily weights, urine specific gravity
• Interventions
• Deficient Fluid Volume
• Activity Intolerance
• Ineffective Therapeutic Regimen Management
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Syndrome of Inappropriate
Antidiuretic Hormone
• Etiology
• Water imbalance related to an increase in ADH synthesis or
secretion, or both
• Pathophysiology
• When ADH is elevated despite normal or low serum osmolality,
kidneys retain excessive water
• Plasma volume expands, causing the blood pressure to rise.
Body sodium is diluted (hyponatremia), and water intoxication
develops
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Syndrome of Inappropriate
Antidiuretic Hormone
• Signs and symptoms
• Weakness, muscle cramps or twitching, anorexia,
nausea, diarrhea, irritability, headache, and weight
gain without edema
• When the central nervous system is affected by
water intoxication, the level of consciousness
deteriorates
• Patient may have seizures or lapse into a coma
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Syndrome of Inappropriate
Antidiuretic Hormone
• Medical diagnosis
• Laboratory tests of serum and urine electrolytes and
osmolality
• Radiographic studies of brain and lungs detect
causative factors
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Syndrome of Inappropriate
Antidiuretic Hormone
• Medical treatment
• Acutely ill: hypertonic saline, very slowly over 4- to
6-hour period
• Restrict fluids to 800-1000 mL/day with high intake
of dietary sodium
• Or administer normal saline with loop diuretics
• Patients who cannot adhere to fluid restriction with
high sodium intake may be given demeclocycline or
lithium carbonate
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Syndrome of Inappropriate
Antidiuretic Hormone
• Assessment
• Anorexia, nausea, vomiting, diarrhea, headache, irritability,
and muscle cramps and weakness
• History of cancer, pulmonary disease, nervous system
disorders, hypothyroidism, or lupus erythematosus
• Note prescription drugs the patient is taking
• Weight, intake and output, urine specific gravity
• Palpate the skin for moisture and edema
• Test muscle strength
• Seizures and muscle weakness, twitching, or cramps
• Describe mental status
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Syndrome of Inappropriate
Antidiuretic Hormone
• Interventions
• Risk for Injury
• Excess Fluid Volume
• Ineffective Therapeutic Regimen Management
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The Adrenal Glands
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Anatomy and Physiology
• A pair of small, highly vascularized triangular-shaped
organs
• Located in the retroperitoneal cavity on the superior
poles of each kidney, lateral to the lower thoracic and
upper lumbar vertebrae
• Each weighs about 4 g and measures 3.3 cm
• Two parts: an outer portion called the cortex and an
inner portion called the medulla
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Anatomy and Physiology
• Medulla
• Constitutes 10% of the gland and contains
sympathetic ganglia with secretory cells
• Stimulation of sympathetic nervous system: medulla
secretes two catecholamines: norepinephrine
(noradrenaline) and epinephrine (adrenaline)
• Function of these substances is adaptation to stress,
as characterized by the “fight-or-flight response,”
and maintenance of homeostasis
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Anatomy and Physiology
• Cortex
• Comprises 90% of adrenal gland; the outer portion
• Considered part of the endocrine system
• Essential for maintaining many life-sustaining physiologic
activities
• Cells organized into three distinct layers or zones
• Zona glomerulosa, zona fasciculata, and zona reticularis
• Hormones synthesized and secreted by cortex are steroids
and consist of mineralocorticoids, glucocorticoids, and
androgens or estrogens
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Function of the Adrenal Glands
• Mineralocorticoids
• Produced by the zona glomerulosa
• Key in maintaining adequate extracellular fluid volume
• Renin, angiotensin, and aldosterone
• Renin produced by juxtaglomerular cells of renal afferent
arterioles
• Release stimulated by decrease in extracellular fluid volume
• Renin acts on plasma proteins to release angiotensin I, which
is catalyzed in the lung to angiotensin II
• Angiotensin II stimulates the secretion of aldosterone, which
results in sodium and water retention
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Function of the Adrenal Glands
• Glucocorticoids
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Produced by the zona reticularis and zona fasciculata
Most abundant and potent is cortisol
92% of circulating cortisol bound to a plasma protein
Cortisol has a permissive effect on other physiologic
processes: the glucocorticoid must be present for other
processes, such as catecholamine activity and excitability of
the myocardium, to occur
• Control of carbohydrate, lipid, and fat metabolism, regulation of
anti-inflammatory and immune responses, and control of
emotional states
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Function of the Adrenal Glands
• Sex hormones
• Adrenal androgens: class of steroids produced in the zona
fasciculata and zona reticularis
• Primary function is masculinization
• Other sex hormones: estrogen and progesterone
• In men, these contribute little to reproductive maturation
• In women, however, estrogens are supplied by the ovaries and
adrenal glands
• In postmenopausal women, the adrenal cortex is the primary
source of endogenous estrogen
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Health History
• Present illness
• Decreased energy, mental changes (depression, anxiety,
nervousness, confusion), sexual dysfunction, gastrointestinal
disturbances, and abnormal skin pigmentation
• Past medical history
• Significant aspects: radiation to the head or abdomen,
intracranial surgery, recent and current medications
• Tuberculosis is the most common cause of primary adrenal
insufficiency
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Health History
• Review of systems
• Patient’s perception of his/her general state of health
• Changes in skin color, especially bronzed or smoky
pigmentation, and increased facial hair in women. Note
changes in weight and appetite
• Headache, lightheadedness with position changes, muscle
weakness, nausea, vomiting, abdominal pain, anorexia,
menstrual dysfunction, erectile dysfunction
• Functional assessment
• Usual diet and activity patterns; disruptions in lifestyle
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Physical Examination
• Height, weight, and vital signs
• Note patient’s responses and ability to follow instructions
• Skin: bronzed/smoky pigmentation, bruising, petechiae, vitiligo,
pallor
• Inspect the face of the female patient for excess facial hair
• Examine the oral mucous membranes for color changes
• Inspect the anterior thorax for fat pads under the clavicles, and the
posterior thorax for the “buffalo hump”
• Obesity of the trunk
• Examine the breasts for striae and darkening of the areola
• Inspect abdomen for striae; extremities for muscle wasting and
edema
• Atrophy, hair loss, appropriateness for age of genitalia
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Age-Related Changes
• Under normal circumstances, adrenal function remains
adequate in older person
• Some decline in cortisol secretion, but this is balanced
by decrease in cortisol metabolism such that blood
levels remain normal
• Secretion of aldosterone and plasma renin activity
decline, thus abilities to conserve sodium and adapt to
position changes less efficient
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Adrenal Hypofunction
• Etiology
• Primary adrenal insufficiency
• Also called Addison’s disease
• Destructive disease process affecting the adrenal glands;
results in deficiencies of cortisol and aldosterone
• Secondary adrenal insufficiency
• A result of dysfunction of the hypothalamus or pituitary that
leads to decreased androgen and cortisol production
• Aldosterone may be affected
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Adrenal Hypofunction
• Pathophysiology
• Insufficiency of adrenocortical steroids: defects associated with
the loss of mineralocorticoids and glucocorticoids
• Impaired secretion of cortisol: decreased gluconeogenesis and
decreased liver and muscle glycogen
• Signs and symptoms
• Progressive weakness, lethargy, unexplained abdominal pain,
and malaise
• Skin hyperpigmentation
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Adrenal Hypofunction
• Acute adrenal crisis (addisonian crisis)
• A life-threatening emergency
• From sudden marked decrease in available adrenal
hormones
• Precipitating factors are adrenal surgery, pituitary
destruction, abrupt withdrawal of steroid therapy,
and stress
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Adrenal Hypofunction
• Acute adrenal crisis (addisonian crisis)
• Manifestations include symptoms of
mineralocorticoid and glucocorticoid deficiency but
are more severe: hypotension, tachycardia,
dehydration, confusion, hyponatremia,
hyperkalemia, hypercalcemia, and hypoglycemia
• If untreated, fluid and electrolyte imbalances can
lead to circulatory collapse, cardiac arrhythmias,
cardiac arrest, coma, and death
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Adrenal Hypofunction
• Medical diagnosis
• Laboratory studies
• Low serum and urinary cortisol level, decreased fasting glucose,
hyponatremia, hyperkalemia, and increased BUN
• Urinary 17-hydroxycorticosteroids
• Plasma ACTH concentration
• Plasma cortisol levels
• Electrocardiogram
• Radiographic studies
• Skull films, arteriograms, CT scans, and MRI
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Adrenal Hypofunction
• Medical treatment
• Replacement therapy with glucocorticoids and
mineralocorticoids
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Adrenal Hypofunction
• Assessment
• Weight loss, salt craving, nausea and vomiting,
abdominal cramping and diarrhea, muscle
weakness and aches, poor stress response,
decreased libido, and amenorrhea
• Pale skin with bronzed areas, emaciation, sparse
body hair, poor skin turgor, hypotension, and muscle
wasting
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Adrenal Hypofunction
• Interventions
• Ineffective Tissue Perfusion
• Risk for Injury
• Imbalanced Nutrition: Less Than Body
Requirements
• Fatigue
• Disturbed Body Image
• Ineffective Management of Treatment Regimen
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Adrenal Hypersecretion
(Cushing’s Syndrome)
• Etiology
• Production of excess amounts of corticosteroids, particularly
glucocorticoid
• Overproduction: endogenous (internal) as well as exogenous
(external)
• Endogenous causes: corticotropin-secreting pituitary tumors, a
cortisol-secreting neoplasm within the adrenal glands, excess
secretion of corticotropin by carcinoma of the lung or other tissues
• Exogenous cause: prolonged administration of high doses of
corticosteroids
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Adrenal Hypersecretion (Cushing’s
Syndrome): Pathophysiology
• Clinical manifestations affect most body systems;
excess levels of circulating corticosteroids
• Produces marked changes in personal appearance,
including obesity, facial redness, hirsutism, menstrual
disorders, hypertension of varying degrees, muscle
wasting of extremities
• Additionally delayed wound healing, insomnia,
irrational behavior, and mood disturbances such as
irritability and anxiety
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Figure 44-6
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Adrenal Hypersecretion (Cushing’s
Syndrome): Pathophysiology
• Findings that lead to diagnosis
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Truncal obesity
Protein wasting
Facial fullness, often called a “moon face”
Purple striae on the abdomen, breasts, buttocks, or
thighs
• Osteoporosis
• Hypokalemia of uncertain etiology
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Adrenal Hypersecretion
(Cushing’s Syndrome)
• Medical diagnosis
• Laboratory studies
• 24-hour urine collection for free cortisol
• Low-dose dexamethasone suppression test
• Abnormal laboratory findings: polycythemia, hypokalemia,
hypernatremia, hyperglycemia, leukocytosis, glycosuria,
hypocalcemia, and elevated plasma cortisol
• Radiographic studies
• CT scan and MRI
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Adrenal Hypersecretion
(Cushing’s Syndrome)
• Medical treatment
• Drug therapy
• Mitotane (Lysodren), ketoconazole (Nizoral),
aminoglutethimide (Cytadren), and metyrapone
(Metopirone)
• Radiation
• Administered externally or internally
• Surgical management
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Adrenal Hypersecretion
(Cushing’s Syndrome)
• Assessment
• Detailed history and physical examination
• Onset of symptoms, prior treatments, drug allergies, and
current medications
• Interventions
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•
•
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Risk for Infection
Disturbed Thought Processes
Risk for Impaired Skin Integrity
Risk for Injury
Disturbed Body Image
Ineffective Therapeutic Regimen Management
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Preoperative Care of the
Adrenalectomy Patient
• Correct any electrolyte imbalances
• Strict hand washing and observance of aseptic
technique to prevent infections in these
susceptible patients
• Preoperative education involves a discussion
of glucocorticoid replacement therapy,
including dosage, side effects, and
complications
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Postoperative Care of the
Adrenalectomy Patient
• Vital signs for signs and symptoms of
impending shock (evident as hypotension),
weak or thready pulse, decreased urinary
output, and changes in level of consciousness
• Pulse and blood pressure may be unstable for
24 to 48 hours after surgery; vasopressors to
maintain blood pressure in immediate
postoperative period
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Postoperative Care of the
Adrenalectomy Patient
• Protect patient by using strict aseptic technique
for wound care and invasive procedures
• Assess comfort at frequent intervals, and treat
pain with opioid analgesics
• Instruct the patient to turn, cough, deep
breathe, or use an incentive spirometer
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Pheochromocytoma
• Usually benign tumor of adrenal medulla
causes excessive catecholamine secretion
• Hypertension, hypermetabolism,
hyperglycemia
• Episodes triggered by emotional distress,
exercise, manipulation of the tumor, postural
changes, and major trauma, including surgery
• Treated by surgical removal of the tumor
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