Pituitary and Adrenal Disorders

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Chapter 44

• Pituitary and Adrenal Disorders

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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 bodys 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 glands weight
• Called the adenohypophysis
• Secretes
• 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
  persons 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
• 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
• 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
• 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
• 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 patients 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
• 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
• Patients 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 patients 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 Addisons 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 (Cushings 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 (Cushings 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 (Cushings Syndrome)
Pathophysiology

• Findings that lead to diagnosis
• 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 (Cushings 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 (Cushings 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 (Cushings Syndrome)

• Assessment
• Detailed history and physical examination
• Onset of symptoms, prior treatments, drug
  allergies, and current medications
• Interventions
• 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