Transcript Chapter 34 - Faculty Sites

Endocrine:
Pituitary and adrenal
Disorders
Nancy Pares, RN, MSN
Metro Community College
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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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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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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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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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Posterior lobe
◦ The smaller lobe
◦ Also called the neurohypophysis
◦ Secretes
 Antidiuretic hormone (ADH), or vasopressin
 Oxytocin
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Present illness
◦ Slowed or accelerated growth, visual disturbances,
headache, and changes in urine output, appearance, skin,
and secondary sex characteristics
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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
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Family history of diabetes insipidus
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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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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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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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In healthy older adults, pituitary function
remains adequate
Increased ADH secretion impairs ability to
concentrate urine, increasing risk of
dehydration
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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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Figure 44-2
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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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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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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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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
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Interventions
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Disturbed Body Image
Activity Intolerance
Chronic Pain
Ineffective Therapeutic Regimen Management
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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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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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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
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Panhypopituitarism
◦ Growth has been completed and some pathologic process
impairs the function of the pituitary
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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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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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Medical diagnosis
◦ Health history, physical examination, diagnostic
tests
◦ Conventional radiographs and CT scans
◦ Cerebral angiography
◦ Serum levels of pituitary hormones
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Medical and surgical treatment
◦ Deficient hormones are replaced as needed
◦ If caused by tumor, surgery, or radiation
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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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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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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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Pathophysiology
◦ Antidiuretic hormone deficiency or inability of kidneys to
respond to ADH results in the excretion of large volumes
of very dilute urine
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Signs and symptoms
◦ Massive diuresis, dehydration, and thirst
◦ Malaise, lethargy, and irritability
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Medical diagnosis
◦ Health history, physical examination, and laboratory
findings
◦ 24-hour urine output of greater than 4 L of fluid
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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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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
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Interventions
◦ Deficient Fluid Volume
◦ Activity Intolerance
◦ Ineffective Therapeutic Regimen Management
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Etiology
◦ Water imbalance related to an increase in ADH synthesis
or secretion, or both
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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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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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Medical diagnosis
◦ Laboratory tests of serum and urine electrolytes
and osmolality
◦ Radiographic studies of brain and lungs detect
causative factors
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Medical treatment
◦ Acutely ill: hypertonic saline, very slowly over 4to 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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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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Interventions
◦ Risk for Injury
◦ Excess Fluid Volume
◦ Ineffective Therapeutic Regimen Management
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A pair of small, highly vascularized triangularshaped 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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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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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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Mineralocorticoids
◦ Produced by the zona glomerulosa
◦ Key in maintaining adequate extracellular fluid volume
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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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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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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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Present illness
◦ Decreased energy, mental changes (depression, anxiety,
nervousness, confusion), sexual dysfunction,
gastrointestinal disturbances, and abnormal skin
pigmentation
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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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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
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Functional assessment
◦ Usual diet and activity patterns; disruptions in lifestyle
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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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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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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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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
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Signs and symptoms
◦ Progressive weakness, lethargy, unexplained abdominal
pain, and malaise
◦ Skin hyperpigmentation
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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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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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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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Medical treatment
◦ Replacement therapy with glucocorticoids and
mineralocorticoids
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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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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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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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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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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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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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Medical treatment
◦ Drug therapy
 Mitotane (Lysodren), ketoconazole (Nizoral),
aminoglutethimide (Cytadren), and metyrapone
(Metopirone)
◦ Radiation
 Administered externally or internally
◦ Surgical management
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Assessment
◦ Detailed history and physical examination
◦ Onset of symptoms, prior treatments, drug allergies, and
current medications
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Interventions
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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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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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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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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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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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Anatomy and physiology
◦ Located in lower portion of the anterior neck
◦ Two lobes, one on each side of trachea
◦ Lobes connected in front of trachea by a narrow
bridge of tissue called the isthmus
◦ Plays a major role in regulating the body’s rate of
metabolism and growth and development
◦ Produces thyroid hormone, triiodothyronine,
calcitonin
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Figure 45-1
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Increased incidence of thyroid nodules
Serum levels of T4 remain approximately the
same in a healthy older person, but levels of
T3 often decline
Incidence of hypothyroidism increases with
age, especially among women
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Health history
◦ Changes in energy level, sleep patterns,
personality, mental function, emotional state
◦ Unexplained weight changes
◦ In the review of systems, changes in menstrual
cycles, sexual function, hydration, bowel
elimination pattern, and tolerance of heat and
cold
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Physical examination
◦ Vital signs and height and weight
◦ Facial expression and characteristics as well as mental
alertness
◦ Inspect/palpate skin for moisture, temperature, texture
◦ Hair texture
◦ Examine the eyes for exophthalmos (bulging)
◦ Inspect the neck for enlargement typical of goiter.
Observe the hands for tremor
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
Diagnostic tests and procedures
◦
◦
◦
◦
◦
Serum T3, free T4, T4, and TSH
Thyroid-releasing hormone (TRH) stimulation test
Radioactive iodine (RAI) uptake test
Thyroid ultrasonography
MRI or CT
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

Abnormally increased synthesis and
secretion of thyroid hormones
Graves’ disease
◦ Most common type of hyperthyroidism
◦ Autoimmune disorder
◦ Antibodies activate TSH receptors, which in turn
stimulate thyroid enlargement and hormone
secretion
◦ Most often develops in young women
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





Often in women in their 60s and 70s
Likely develop in people who have had
goiter for a number of years
Caused by small thyroid nodules that
secrete excess thyroid hormone
Increased hormone production is
independent of TSH
Nodules can be benign or malignant
Symptoms are usually less severe
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

Weight loss and nervousness with a mild form
In more severe cases
◦ Restlessness, irritable behavior, sleep disturbances, emotional
lability, personality changes, hair loss, and fatigue
◦ Weight loss, even when the patient is eating well, is common
◦ Poor tolerance of heat and excessive perspiration
◦ Changes in menstrual and bowel patterns
◦ Warm, moist, velvety skin; fine hand tremors; swelling of the
neck; and ophthalmopathy including exophthalmos
◦ Tearing, light sensitivity, decreased visual acuity, and swelling
around orbit of the eye
◦ Tachycardia, increased systolic blood pressure, sometimes atrial
fibrillation
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Figure 45-2
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
Thyrotoxicosis
◦ Excessive stimulation caused by elevated thyroid
hormone levels that produce dangerous
tachycardia and hyperthermia
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

Decreased TSH and elevated serum T4
Measurement of thyroid-stimulating
antibodies and results of a radioactive
iodine uptake test to diagnose Graves’
disease
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
Drug therapy
◦ Antithyroid drugs
 Thionamides and iodides

Radioactive iodine
◦ Accumulates in the thyroid gland, where it causes
destruction of thyroid tissue

Surgical treatment
◦ Subtotal thyroidectomy
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
Assessment
◦ Activity tolerance, heat tolerance, bowel
elimination pattern, appetite, weight changes, and
food intake
◦ Mental-emotional state, adaptation to the
condition, and understanding of the treatment
◦ Measure vital signs and height and weight
◦ Skin texture and edema
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






Decreased Cardiac Output
Disturbed Sleep Pattern
Hyperthermia
Imbalanced Nutrition: Less Than Body
Requirements
Risk for Injury
Disturbed Sensory Perception
Diarrhea
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
Assessment: preoperative
◦ Identify and address learning needs
◦ Teaching: primary preoperative nursing intervention
◦ Goals: understanding of the usual preoperative and
postoperative procedures and decreased anxiety

Assessment: postoperative
◦ Assess and document respiratory status, level of
consciousness, wound drainage or bleeding, voice quality,
comfort, and neuromuscular irritability
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
Interventions
◦
◦
◦
◦
◦
Ineffective Airway Clearance
Decreased Cardiac Output
Disturbed Body Image
Acute Pain
Risk for Infection
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

Inadequate secretion of thyroid hormones
Cretinism
◦ If not treated early, hypothyroidism during infancy causes
permanent physical and mental retardation


In adults can be serious but usually reversible
with treatment
Myxedema
◦ Facial edema from severe, long-term hypothyroidism
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Figure 45-4
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Figure 45-5
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
Primary
◦ Atrophy of the thyroid gland after years of Graves’
disease or thyroiditis
◦ Treatment for hyperthyroidism
◦ Dietary iodine deficiency
◦ High intake of goitrogens
◦ Defects in thyroid hormone synthesis

Secondary
◦ Pituitary or hypothalamic disorders
◦ Thyroidectomy
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







Swelling of the lips and eyelids
Dry, thick skin
Bruising
Thin, coarse hair
Hoarseness
Generalized nonpitting edema
Facial edema
May seem slow, depressed, or apathetic
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

Based on laboratory determination of free T4
and TSH
Complications
◦ Myxedema coma

Medical treatment
◦ Hormone replacement therapy
 Levothyroxine (Synthroid) or liothyronine (Cytomel)
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








Activity Intolerance
Imbalanced Nutrition: More Than Body
Requirements
Hypothermia
Constipation
Risk for Impaired Skin Integrity
Decreased Cardiac Output
Disturbed Thought Processes
Disturbed Body Image
Self-Care Deficit
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
Thyroid enlargement with normal hormone
production
◦ Causes
 Iodine deficiency and long-term exposure to
goitrogens
 The gland may enlarge to compensate for
hypothyroidism
 Sometimes the enlarged gland produces excess
hormones, making the patient hyperthyroid
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
Treatment
◦ If mild enlargement and normal hormones, no
intervention
◦ Some patients need hormone replacement therapy
◦ Surgery indicated if pressure on the trachea or
esophagus or if the condition is disfiguring
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Figure 45-6
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
Nodules
◦ Can be benign or malignant
◦ Physician may order a scan that uses radioactive
iodine; determines cancer
◦ Nodular goiters usually surgically removed
◦ In benign conditions, only the nodule may be
removed
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





Uncommon
Fatal in less than 1% of all cases
Early stages: nodule that can be felt on thyroid
If cancer spreads, enlarged lymph nodes felt in
the neck
Patient may not show dramatic changes in thyroid
hormone levels
Total thyroidectomy is the usual treatment
◦ If malignancy spreads beyond thyroid gland, more radical
surgery may be indicated
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
Small glands located on back of thyroid
◦ Occasionally found in the mediastinum as well



Usually 4 parathyroids; some people have more
Embedded in thyroid, but function independently
Secrete only one hormone, but it is vital
◦ Parathyroid hormone, or parathormone (PTH), plays a
critical role in regulating the serum calcium level
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Figure 45-7
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
Health history
◦ Change in mental-emotional status, such as memory
problems, irritability, or personality changes
◦ Musculoskeletal problems, including weakness, skeletal
pain, backache, and muscle twitching or spasms
◦ Urinary frequency, polyuria, urinary calculi (stones), or
constipation
◦ Head/neck radiation, renal calculi, chronic renal failure
◦ Medications, including calcium and vitamin D
supplements
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
Physical examination
◦ Heart rate and rhythm, blood pressure, respiratory
effort, muscle strength, muscle twitching, and hair
and skin texture
◦ Chvostek’s sign
 Spasm of facial muscle when facial nerve tapped
◦ Trousseau’s sign
 Carpopedal spasm when a blood pressure cuff is
inflated above the patient’s systolic blood pressure
and left in place for 2 to 3 minutes
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Figure 45-3
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
Blood tests
◦ Calcium, phosphate, creatinine, uric acid,
magnesium, alkaline phosphatase, and PTH



Radiographs
Dental examination
Electrocardiogram
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

Secretion of excess parathormone (PTH)
Causes
◦ Tumor (an adenoma); can be benign or malignant
◦ Vitamin D deficiencies, malabsorption, chronic renal
failure, and elevated serum phosphate


Elevation of serum calcium (hypercalcemia)
High levels of PTH cause calcium to shift from the
bones into the bloodstream
◦ If untreated, severe demineralization of bone tissue
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
Symptoms vague at first
◦ Weakness, lethargy, depression, anorexia, and
constipation

Other findings include mental and
personality changes, cardiac dysrhythmias,
weight loss, and urinary calculi
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



Elevated serum calcium and decreased
serum phosphate
Elevated PTH and 24-hour urine calcium
Skeletal radiographs and bone density
studies
CT, MRI, ultrasound, fine-needle aspiration,
and selective arteriography
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
Surgical intervention
◦ Parathyroidectomy
◦ Surgeon attempts to leave some parathyroid
tissue to prevent hypoparathyroidism
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Thyroid and Parathyroid
Disorders
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
Drug therapy
◦ Sodium and phosphorus replacements
◦ Calcitonin (Calcimar), gallium nitrate (Ganite),
bisphosphonates (etidronate, pamidronate), and
plicamycin (Mithracin) inhibit release of calcium
from bones
◦ Furosemide (Lasix): promotes excretion of calcium
in the urine
◦ Propranolol reduces PTH secretion
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
Monitor vital signs, urine output, weight,
muscle strength, bowel elimination, and
digestive disturbances
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




Activity Intolerance and Risk for Injury
Impaired Urinary Elimination
Constipation
Disturbed Thought Processes
Imbalanced Nutrition: Less Than Body
Requirements
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
Airway obstruction from accumulated fluid and
blood in surgical site compressing the trachea
◦ Monitor and document the respiratory rate and effort and
the pulse rate
◦ Increasing pulse and respiratory rates, especially
accompanied by restlessness, suggest inadequate
oxygenation
◦ Notify physician of indications of respiratory distress
◦ Keep an emergency tracheotomy tray at the bedside in
the event of acute obstruction
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

Airway obstruction related to severe
hypocalcemia
Be alert for tetany
◦ Tingling around mouth and in the fingers
◦ It may progress to severe muscle spasms or
cramps and even to laryngospasm
◦ Treated with oral or intravenous calcium
supplements
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



Protect suture line from stress
Show patient how to support the head when
changing positions
Inspect dressing and back of the neck for
bleeding
Elevate patient’s head to reduce swelling
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




Deficiency of parathormone (PTH)
Uncommon condition
From accidental removal of/damage to parathyroid glands
during surgery
Primary hypoparathyroidism can be caused by an
autoimmune process and by several conditions, including
Wilson’s disease (copper overload)
Inadequate secretion of PTH leads to hypocalcemia
◦ Severe hypocalcemia can progress to convulsions and
respiratory obstruction due to spasms of the larynx
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
Signs and symptoms
◦ Painful muscle cramps, fatigue and weakness,
tingling and twitching of the face and hands,
mental and emotional changes, dry skin, and
urinary frequency
◦ With severe hypocalcemia, difficulty breathing,
convulsions, and cardiac dysrhythmias
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
Medical diagnosis
◦ Low serum calcium, elevated serum phosphate, low urine
calcium, and sometimes low serum magnesium
◦ Chvostek’s sign and Trousseau’s sign

Medical treatment
◦ Acute hypoparathyroidism: sometimes parenteral PTH
◦ Severe hypocalcemia: with intravenous calcium salts
◦ Chronic hypoparathyroidism: with oral calcium salts and a
form of vitamin D
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
Interventions
◦ Administer drugs as ordered
◦ If recent seizure activity or if patient shows severe
neuromuscular irritability, follow seizure precautions
◦ Pulse/blood pressure for dysrhythmias/heart failure
◦ Teach signs and symptoms of calcium imbalances, and
provide instructions for self-medication
◦ Advise patient to carry medical ID card to alert health care
providers in event of an emergency
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Diabetes Mellitus
and Hypoglycemia
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

Chronic disorder of impaired metabolism
with vascular and neurologic complications
Key feature is elevated blood glucose, called
hyperglycemia
◦ Blood glucose level normally regulated by insulin,
a hormone produced by beta cells in the islets of
Langerhans located in the pancreas
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
Absence of endogenous insulin
◦ Formerly called juvenile-onset diabetes because it most
commonly occurs in juveniles and young adults


An autoimmune process, possibly triggered by a
viral infection, destroys beta cells, the
development of insulin antibodies, and the
production of islet cell antibodies (ICAs)
Affected people require exogenous insulin for the
rest of their lives
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




Inadequate endogenous insulin and body’s
inability to properly use insulin
Beta cells respond inadequately to hyperglycemia;
results in chronically elevated blood glucose
Continuous high glucose level in the blood
desensitizes the beta cells; they become less
responsive to the elevated glucose
More common in adults; increasing in children
Controlled by diet and exercise; may require oral
hypoglycemic agents or exogenous insulin
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
Glucose
Insulin stimulates active transport of glucose into cells
If insulin absent, glucose remains in the bloodstream
Blood becomes thick, which increases its osmolality
Increased osmolality stimulates the thirst center
Increased fluid does not pass into body tissues; high
serum osmolality retains fluid in the bloodstream
◦ As blood passes through the kidneys, some glucose
eliminated
◦ Osmotic force created by glucose draws extra fluid and
electrolytes with it, causing abnormally increased urine
volume
◦
◦
◦
◦
◦
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
Fatty acids
◦ Promotes fatty acid synthesis and conversion of fatty
acids into fat, which is stored as adipose tissue
◦ Also spares fat by inhibiting breakdown of adipose tissue
and mobilization of fat and by inhibiting the conversion
of fats to glucose
◦ Without adequate insulin, fat stores break down and
increased triglycerides are stored in the liver
◦ Increased fatty acids in the liver can triple the production
of lipoproteins; promotes atherosclerosis
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
Protein
◦ Enhances protein synthesis in tissues and inhibits the
conversion of protein into glucose
◦ Amino acids are admitted into cells; enhances rate of
protein formation while preventing protein degradation
◦ Without adequate insulin, protein storage halts; large
amounts of amino acids dumped into the bloodstream
◦ High levels of plasma amino acids place people with
diabetes at risk for development of gout
◦ Changes in protein metabolism lead to extreme weakness
and poor organ functioning
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

An autoimmune malfunction may cause
complete destruction of the islets of
Langerhans in the pancreas, creating type 1
diabetes
Islet cell antibodies are identified in more
than 80% of all people with type 1 diabetes
at the time of diagnosis
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Figure 46-1
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








Obesity
Sedentary lifestyle
Family history of diabetes
Age 40 years and older
History of gestational DM
History of delivering infant weighing more than 10 lb
African American (33% higher risk for type 2 DM)
Latin American/Hispanic (>300% higher risk for type 2 DM)
American Indians (33%-50% higher risk for type 2 DM)
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
Metabolic syndrome
◦ Thought to be a precursor to diabetes
◦ Impaired glucose tolerance, high serum insulin,
hypertension, elevated triglycerides, low HDL cholesterol,
altered size and density of LDL cholesterol
◦ Believed that metabolic syndrome is a chronic low-grade
inflammatory process affecting endothelial tissue
◦ Long-term effects: atherosclerosis, ischemic heart
disease, left ventricular hypertrophy, type 2 DM
◦ Research directed at learning how to detect this syndrome
early and what interventions might slow or arrest the
progress
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Retinopathy
◦ Pathological changes in the retina that are
associated with DM

Nephropathy
◦ Kidney damage
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

Accelerated atherosclerotic changes in the
person with diabetes
Associated with coronary artery disease
(CAD), cerebral vascular accidents (CVA or
stroke), and peripheral vascular disease
(PVD)
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
Neuropathy: pathologic changes in nerve
tissue
◦ Mononeuropathy affects a single nerve or group
of nerves
◦ Polyneuropathy involves both sensory and
autonomic nerves
◦ Autonomic neuropathy affects the sympathetic
and parasympathetic nervous systems
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

The usual symptoms of tachycardia,
palpitations, tremor, sweating, and
nervousness may be absent
Patient may suddenly have changes in
mental status as the first sign of
hypoglycemia
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
Foot complications of diabetes
◦ May have foot problems associated with
neuropathy, inadequate blood supply, or a
combination
◦ Mechanical irritation
◦ Thermal injury
◦ Chemical irritation
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

Diabetes Control and Complications Trial
(DCCT): intensive treatment of type 1 DM
delayed the onset or slowed the progress of
diabetic retinopathy, nephropathy, and
neuropathy
Outcome of United Kingdom Prospective
Diabetes Study (UKPDS): similar benefits of
tight control with type 2 DM
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
ADA recommends
◦
◦
◦
◦
◦
Blood pressure: <130 systolic, <80 diastolic
Total cholesterol: <200 mg/dL
LDL: <100 mg/dL
HDL: >45 mg/dL for men (>55 mg/dL for women)
Triglyceride: <150 mg/dL
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

Dangerous drop in blood glucose
Causes
◦ Taking too much insulin, not eating enough food or not
eating at the right time, an inconsistent pattern of
exercise
◦ Gastroparesis, renal insufficiency, and certain drugs
including aspirin and beta-adrenergic blockers
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
Signs and symptoms
◦ Adrenergic: shakiness, nervousness, irritability,
tachycardia, anxiety, lightheadedness, hunger, tingling or
numbness of the lips or tongue, and diaphoresis
◦ Neuroglucopenia: drowsiness, irritability, impaired
judgment, blurred vision, slurred speech, headaches, and
mood swings progressing to disorientation, seizures, and
unconsciousness
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
Treatment
◦ Give patient 10 to 15 g of quick-acting
carbohydrates
◦ Repeat every 15-30 minutes until blood glucose is
>70 mg/dL for adults, 80 to 100 mg/dL for older
adults and children
◦ If patient is unable to swallow, an IM or
subcutaneous injection of 1 mg of glucagon or an
IV dose of 50 mL of 50% dextrose should be given
as ordered or per protocol
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

Life-threatening emergency caused by a relative
or absolute deficiency of insulin
Early signs and symptoms
◦ Anorexia, headache, and fatigue
◦ As condition progresses, classic symptoms of polydipsia,
polyuria, and polyphagia develop

If untreated, patient becomes dehydrated, weak,
and lethargic with abdominal pain, nausea,
vomiting, fruity breath, increased respiratory rate,
tachycardia, blurred vision, and hypothermia
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
Late signs
◦ Air hunger (Kussmaul’s respirations), coma, and
shock
◦ Death can result without prompt medical care
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
Treatment aimed at correction of three main
problems
◦ Dehydration
◦ Electrolyte imbalance
◦ Acidosis
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
Patient goes into a coma from extremely high
glucose levels (>600 mg/dL)
◦ There is no evidence of elevated ketones
◦ Pancreas produces enough insulin to prevent breakdown
of fatty acids and formation of ketones, but not enough
to prevent hyperglycemia



Persistent hyperglycemia causes osmotic diuresis,
resulting in loss of fluid and electrolytes
Dehydration and hypernatremia develop
May be caused by the same factors that trigger
ketoacidosis
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
One or more of the following criteria on two
separate occasions is considered DM
◦ Polyuria, polydipsia, polyphagia, unexplained weight loss
plus random glucose level >200 mg/dL
◦ Fasting serum glucose level >126 mg/dL (after at least an
8-hour fast)
◦ Two-hour postprandial glucose level >200 mg/dL during
oral glucose tolerance test (OGTT) under specific
guidelines. Test must use a glucose load of 75 g of
anhydrous glucose dissolved in water
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
Prediabetes
◦ Individuals with impaired fasting glucose (IFG)
and/or impaired glucose tolerance (IGT)
◦ Individuals should receive education on weight
reduction and increasing physical activity
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
Oral glucose tolerance test
Diet of 150 to 300 g carbohydrate for 3 days before test
Night before test, patient fasts after midnight
Morning of test, blood drawn for fasting serum glucose
Patient then given a drink (Glucola) containing 75 g of
carbohydrates and instructed to remain quiet
◦ Blood drawn at 30 minutes and 1 hour after the ingestion
of glucose. After these two samples, blood is drawn at
hourly intervals until the test is completed
◦
◦
◦
◦
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Nutritional management
◦ Medical nutrition therapy (MNT) is an important
part of diabetes management; should be included
in diabetes self-management education
 Because of complexity of nutritional management, a
registered dietitian should be part of the diabetes
management team, and the individual with diabetes
should be included in decision making
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
Exercise
◦ Effective adjunct for people with diabetes
◦ Aids in weight loss, improves cardiovascular
conditioning, improves insulin sensitivity, and
promotes a sense of well-being
◦ Exercising muscle uses glucose at 20 times the
rate of a muscle at rest and does not require
insulin
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

All patients with type 1 disease need insulin
injections; some patients with type 2 disease may
eventually need insulin
Insulins classified by source and course of action
◦ Source: human, pork, or beef (beef is being
phased out)
◦ Course of action: rapid acting, short acting,
intermediate acting, and long acting
 All rapid-acting and short-acting insulins are clear
 The other insulins are cloudy
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Figure 46-2
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Route
◦ Oral: insulin cannot be given orally because it is rendered
useless in the gastrointestinal tract
◦ Subcutaneously: all insulins can be given subcutaneously
◦ Intravenously: ONLY regular insulin can be given
intravenously
◦ Inhalation: a form of insulin that can be taken by
inhalation has recently been approved, but it is not yet
widely used
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Concentrations
◦ U-100 insulin has 100 units/mL
 Most commonly used
◦ U-500 insulin has 500 units/mL
 Used only in emergencies and for patients who are
extremely insulin resistant
◦ U-40 insulin has 40 units/mL
 Not available in the United States
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Premixed insulin products
◦ Contain both Regular and NPH insulin
◦ 70% NPH and 30% Regular insulin
◦ 50% NPH and 50% Regular insulin
◦ 75% NPH and 25% Lispro
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Dosing schedules
◦ Conventional therapy
 Typically uses a combination of a short-acting and
an intermediate- or long-acting insulin
◦ Intensive therapy
 To achieve tight control; may require 3 or 4
injections daily
◦ Continuous subcutaneous insulin infusion
 Patient has indwelling subcutaneous catheter
connected to an external portable infusion pump;
pump delivers Regular insulin continuously
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Insulin mixing
◦ Two types can be mixed in one syringe to avoid two
injections
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Insulin injection
◦ Site rotation helps prevent lipohypertrophy or lipoatrophy
◦ Absorption rate varies with different body sites
◦ American Diabetes Association recommends rotating sites
within one anatomic area rather than moving among all
areas
◦ See Figure 46-3
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Figure 46-3
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Insulin pump
◦ Needle is inserted subcutaneously in an
appropriate part of the anatomy
◦ Pump is programmed to deliver a steady trickle of
insulin throughout the day and can provide a
bolus of insulin at mealtimes
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Figure 46-4
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Intranasal route
◦ Only 10% of the drug is absorbed through the nasal
mucosa, making it relatively expensive to use
◦ Nasal irritation is a frequent side effect
◦ Only Regular insulin is given intranasally

Insulin catheter
◦ Indwelling subcutaneous catheters may be placed in the
abdomen to permit repeated insulin injections without
repeated needlesticks
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If patients with type 2 DM unable to control blood
glucose with nutrition and exercise, physician
may prescribe oral hypoglycemics
Sulfonylureas (three generations), alphaglucosidase inhibitors, biguanides,
thiazolidinediones, D-phenylalanines,
meglitinides
Combination oral medications
◦ ACTOplus met (pioglitazone and metformin), Avandamet
(rosiglitazone and metformin), Avandaryl (rosiglitazone
and glimepiride), Glucovance (glyburide and metformin),
Metaglip (glipizide and metformin)
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Allows patients to monitor blood glucose
levels to regulate their diet, exercise, and
medication regimens to remain euglycemic
Portable electronic glucose meters have
largely replaced other methods of selfmonitoring
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Glycosylated hemoglobin (HbA1c) reflects
glucose levels over the past few months
Fructosamine levels reflect those over
several weeks
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Hypoglycemia
◦ A person injects too much insulin, does not eat enough,
eats at the wrong time, or exercises inconsistently: glucose
levels may suddenly drop

Somogyi phenomenon
◦ Rebound hyperglycemia in response to hypoglycemia

Dawn phenomenon
◦ An increase in fasting blood glucose levels between 5 and 9
AM that is not related to hypoglycemia
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Ketoacidosis: ketonuria, Kussmaul’s
respirations, orthostatic hypotension,
hypertension, nausea, vomiting, lethargy, or
change in level of consciousness
Hypoglycemic patient: expect to find
tachycardia, anxiety, trembling, and
decreasing level of consciousness
Be alert for indications of hyperosmolar
nonketotic coma
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Attempt to determine the following
◦ Type of diabetes
◦ Hypoglycemic agents: name, dosage, when last
dose was taken
◦ Food and fluid intake for the past 3 days
◦ Relevant laboratory values: blood glucose, blood
pH, bicarbonate levels, electrolytes, and
osmolality and urine osmolality
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Chief complaint and history of present illness
◦ Signs/symptoms that prompted patient to seek medical
care
Past medical history
◦ Type and duration of DM
◦ Name and dosage of prescribed medications and when
they were last taken
◦ If patient monitors blood glucose, record type of
equipment used, testing schedule, recent test results
Family history
◦ Diabetes, heart disease, stroke, hypertension,
hyperlipidemia
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Review of systems
◦ Description of the patient’s general health
◦ Changes in skin moisture or turgor
◦ Inquire whether the patient has had floaters, diplopia
(double vision), or blurred vision, or has seen white halos
around objects
◦ Abdominal symptoms: diarrhea, abdominal bloating, and
gas
◦ Problems passing or holding urine
◦ If any pain in the legs, note when it occurs
◦ Numbness, tingling, or burning in the extremities
◦ Changes in mental alertness or seizures
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Functional assessment
 Explore factors that can affect patient’s ability to
perform self-care, including literacy, financial
resources such as health insurance, and family
support
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Physical examination
◦ Level of consciousness, posture and gait, and apparent
well-being
◦ Vital signs, height, and weight
◦ Skin color, warmth, turgor, and lesions noted
◦ Inspect eye grounds for evidence of diabetic retinopathy
or cataracts
◦ Be alert for a sweet, fruity odor to the patient’s breath
that is common with ketoacidosis
◦ Carefully assess the feet
◦ Test gait, balance, and motor coordination
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Ineffective Health Maintenance
Ineffective Therapeutic Regimen Management
Risk for Deficient Fluid Volume
Risk for Injury
Activity Intolerance
Chronic Pain
Disturbed Sensory Perception or Impaired Skin
Integrity
Disturbed Thought Processes
Ineffective Coping
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Develops when the blood glucose level falls
to less than 45 to 50 mg/dL
Symptoms occur at different blood levels
according to individual tolerances and how
rapidly the level falls
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Exogenous hypoglycemia
◦ Results from outside factors acting on the body to
produce a low blood glucose
◦ Include insulin, oral hypoglycemic agents, alcohol,
or exercise
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Endogenous hypoglycemia
◦ Occurs when internal factors cause an excessive
secretion of insulin or an increase in glucose
metabolism
◦ These conditions may be related to tumors or
genetics
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Functional hypoglycemia
◦ From a variety of causes, including gastric surgery,
fasting, or malnutrition
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Glucose level falls rapidly, causes epinephrine,
cortisol, glucagon, and growth hormone to be
secreted in an attempt to increase glucose levels
◦ Symptoms: weakness, hunger, diaphoresis, tremors,
anxiety, irritability, headache, pallor, and tachycardia

A blood glucose level that falls over several
hours: symptoms attributed to lack of essential
glucose to brain tissue
◦ Symptoms: confusion, weakness, dizziness, blurred or
double vision, seizure, and in severe cases, coma
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The diagnosis of hypoglycemia not associated
with diabetes can be based on fasting blood
glucose, OGTT, intravenous glucose tolerance
test, and 72-hour inpatient fasting
Whipple’s triad
◦ The presence of symptoms
◦ Documentation of low blood glucose when symptoms
occur
◦ Improvement of symptoms when blood glucose rises
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In an unconscious patient who has diabetes,
hypoglycemia should be suspected until it is
ruled out
◦ 50 mL of 50% glucose solution should be administered
immediately

The patient with a milder form of hypoglycemia
◦ Treated with 15 g carbohydrate
◦ If the patient’s condition does not improve, another
15 g of carbohydrate should be given after 10 minutes
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Prevention of hypoglycemia by proper food intake
◦ The diet is directed by the underlying cause
◦ If overproduction of insulin after carbohydrate ingestion,
a low-carbohydrate, high-protein diet
◦ Restriction of carbohydrates to no more than 100 g/day
is recommended
◦ Simple sugars avoided; complex carbohydrates
encouraged
◦ Patients may tolerate smaller, more frequent meals.
Alcohol should be avoided
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Present illness: shakiness, nervousness, irritability,
tachycardia, anxiety, lightheadedness, hunger,
tingling or numbness of the lips or tongue,
nightmares, and crying out during sleep
Note when episodes occur in relation to meals
and particular food intake
The past medical history documents diabetes,
previous gastric surgery, abdominal cancer, or
adrenal insufficiency
Medications, paying particular attention to
hypoglycemic agents
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Note hypoglycemic agents, prescribed dose,
and the time last dose taken
Functional assessment: information about
current diet, exercise, alcohol intake, and
the effects of symptoms on daily activities
Important aspects of the physical
examination include general behavior,
appearance, pulse, and blood pressure
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Deficient Knowledge
Risk for Injury
Impaired Adjustment
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