CHAPTER 43
DRUGS FOR PITUITARY, THYROID, AND ADRENAL DISORDERS
LEARNING OUTCOME 1
Describe the general structure and functions of the endocrine system.
Concepts
The endocrine system consists of glands that secrete hormones. The endocrine system is a major controller of
homeostasis. It maintains homeostasis by using hormones transported through the blood as chemical
messengers that are secreted in response to changes in the internal environment. The release of hormones is
commonly controlled by negative feedback, and one hormone may control another. (See Figure 43.1.)
Figure 43.1 The Endocrine System
LEARNING OUTCOME 2
Through the use of a specific example, explain the concept of negative feedback in the endocrine system.
Concepts
In negative-feedback loops it is common for the last hormone in a pathway to provide feedback to turn off the
secretion from the first hormone. For example, as serum calcium levels fall, PTH is released; PTH causes an
increase in serum calcium, which provides feedback to the parathyroid glands to shut off PTH secretion. This
characteristic feature of endocrine homeostasis is known as negative feedback. Negative feedback helps to
prevent excessive secretion of hormones thereby limiting their physiologic responses.
LEARNING OUTCOME 3
Describe the clinical applications of the hypothalamic and pituitary hormones.
Concepts
1. The hypothalamus and pituitary glands control many other glands. The hypothalamus secretes releasing
hormones, which direct the anterior pituitary gland as to which hormones should be released. The posterior
pituitary releases its hormones in response to nerve signals from the hypothalamus. (See Figure 43.2 for an
illustration of the hypothalamus and pituitary.)
2. Hormones are used as replacement therapy, as antineoplastics, and for their natural therapeutic effects, such
as their exaggerated response or suppression of body defenses. Hormone blockers are used to inhibit actions
of certain hormones. (See Table 43.1 for examples of hormone pharmacotherapy.)
Figure 43.2 Hormones Associated with the Hypothalamus and the Pituitary Gland
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LEARNING OUTCOME 4
Explain the pharmacotherapy of diabetes insipidus.
Concepts
Antidiuretic hormone (ADH) conserves water in the body. A deficiency in ADH results in diabetes insipidus
(DI), a rare condition characterized by the production of large volumes of very dilute urine, usually
accompanied by increased thirst. Two ADH preparations are available for the treatment of diabetes insipidus:
vasopressin (Pitressin) and desmopressin (DDAVP, Stimate). Vasopressin is a synthetic hormone that has a
structure identical with that of human ADH. It acts on the renal collecting tubules to increase their permeability
to water, thus enhancing water reabsorption. Although it acts within minutes, vasopressin has a short half-life
requiring it to be administered 3 to 4 times per day. Vasopressin tannate is formulated in peanut oil to increase
its duration of action. Vasopressin is usually given IM or IV, although an intranasal form is available for mild
diabetes insipidus. Desmopressin is the most common form of antidiuretic hormone in use. Details regarding
this drug may be found in the Prototype Drug feature.
Table 43.2 Selected Hypothalamic and Pituitary Agents
LEARNING OUTCOME 5
Identify the signs and symptoms of hypothyroidism and hyperthyroidism.
Concepts
1. The thyroid gland secretes thyroxine (T4) and triiodothyronine (T3), which control the basal metabolic rate
and affect every cell in the body. Parafollicular cells in the thyroid secrete calcitonin, which is responsible
for calcium homeostasis. Follicular cells secrete T4 and T3, and iodine is essential for the synthesis of T4 and
T3. A negative-feedback loop controls secretion, and low thyroxine levels signal the hypothalamus to release
thyroid-releasing hormone (TRH), which signals the pituitary to release thyroid-stimulating hormone
(TSH). (This negative feedback for the thyroid is illustrated in Figure 43.3.)
2. Early symptoms of hypothyroidism in adults, or myxedema, include general weakness, muscle cramps, and
dry skin. More severe symptoms include slurred speech, bradycardia, weight gain, decreased sense of taste
and smell, and intolerance to cold environments. Lab results generally reveal elevated TSH with diminished
T3 and T4 levels. Symptoms of hyperthyroidism are increased body metabolism, tachycardia, weight loss,
elevated body temperature, and anxiety.
Figure 43.3 Feedback Mechanisms of the Thyroid Gland
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LEARNING OUTCOME 6
Explain the pharmacotherapy of thyroid disorders.
Concepts
1. The most common cause of hypothyroidism (myxedema) is chronic autoimmune thyroiditis (Hashimoto’s
disease). Lab studies reveal an elevated thyroid-stimulating hormone (TSH) level and decreased T3 and T4
levels. Hypothyroidism may be treated by administering natural or synthetic thyroid hormones, especially
levothyroxine (T4). (See Table 43.3 for a list of medications.)
2. The most common cause of hyperthyroidism is Graves’ disease. The goal of pharmacotherapy is to lower
the activity of the thyroid. Hyperthyroidism is treated by administering agents such as the thioamides, such
as propylthiouracil (PTU) and methimazole (Tapazole), which decrease the activity of the thyroid gland; or
by using a radioactive iodide that kills overactive thyroid cells, such as sodium iodide-131, Lugol’s solution.
Table 43.3 Thyroid and Antithyroid Drugs
LEARNING OUTCOME 7
Describe the signs and symptoms of Addison’s disease and Cushing’s syndrome.
Concepts
1. The adrenal cortex secretes glucocorticoids, gonadocorticoids, and mineralocorticoids. The glucocorticoids
mobilize the body for long-term stress and influence carbohydrate, lipid, and protein metabolism in most
cells. Mineralocorticoids promote sodium reabsorption and potassium secretion. Gonadocorticoids include
male sex hormones (androgens).
2. Addison’s disease is primary adrenocortical insufficiency. It is rare and includes a deficiency of both
glucocorticoids and mineralocorticoids. Symptoms include nausea, vomiting, lethargy, confusion, and
coma. Low plasma cortisol, accompanied by high plasma ACTH levels, is diagnostic because this indicates
the adrenal gland is not responding to ACTH stimulation.
3. Cushing’s syndrome occurs when high levels of glucocorticoids are present in the body over a prolonged
period. Signs and symptoms include adrenal atrophy, osteoporosis, hypertension, increased risk of
infections, delayed wound healing, acne, peptic ulcers, general obesity, and a redistribution of fat around
the face (moon face), shoulders, and neck (buffalo hump). Mood and personality changes may occur.
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LEARNING OUTCOME 8
Explain the pharmacotherapy of adrenal gland disorders.
Concepts
1. Control of glucocorticoid levels in the blood begins with corticotropin-releasing factor (CRF), secreted by
the hypothalamus. CRF travels to the pituitary, where it causes the release of adrenocorticotropic hormone
(ACTH). ACTH then travels through the blood and reaches the adrenal cortex, causing it to release
glucocorticoids. When the level of cortisol in the blood rises, it provides negative feedback to the
hypothalamus and pituitary to shut off further release of glucocorticoids. (This negative-feedback
mechanism is shown in Figure 43.4.) Adrenocorticotropic hormone (ACTH) and related agents are rarely
used as medications. They must be given parenterally and have many side effects. Their primary use is to
diagnose adrenal disorders.
2. Adrenocortical insufficiency may be acute or chronic. Glucocorticoids are prescribed for primary
(Addison’s disease) and secondary adrenocortical insufficiency, allergies, neoplasms, and a wide variety of
other conditions. (See Table 43.4 for a listing of medications.)
3. Antiadrenal drugs may be used to treat severe Cushing’s syndrome, which occurs with prolonged
glucocorticoid therapy by inhibiting corticosteroid synthesis. Antiadrenal drugs are not curative, and their
use is usually limited to 3 months of therapy.
Figure 43.4 Feedback Control of the Adrenal Cortex
Table 43.4 Selected Glucocorticoids
ANIMATIONS AND VIDEOS

Pharmacotherapy Illustrated 43.1
LEARNING OUTCOME 9
Describe the nurse’s role in the pharmacologic management of pituitary, thyroid, and adrenal disorders.
Concepts
1. The role of the nurse in the pharmacologic management of pituitary, thyroid, and adrenal disorders involves
careful monitoring of a client’s condition and providing education as it relates to the prescribed drug
treatment. Obtain baseline medical, surgical, and drug history; lifestyle and dietary habits, including use of
herbal or alternative therapies; and a detailed description of symptomology and current therapies.
2. Antidiuretic hormone therapy for ADH deficiency: Assess for electrolyte imbalances and changes in
specific gravity and fluid intake. Monitor serum sodium and potassium levels. Monitor urinary specific
gravity, routine urinalysis, body weight, and fluid intake and output. Assess vital signs, especially blood
pressure and pulse. Assess neurological status for symptoms of headache and changes in mental status such
as drowsiness and confusion. Advise clients to avoid alcohol.
3. Thyroid hormone therapy: Assess the client’s weight and vital signs. Assess tachycardia, irregular heart
rate, hypertension, nervousness, weight loss, diarrhea, and heat intolerance, which could indicate an
overdose of thyroid hormone. Monitor clients with impaired renal function closely. Monitor for excess
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fatigue, slow speech, hoarseness or slow pulse, because these may indicate underdosage.
4. Hypothyroidism therapy: Assess for signs and symptoms of hypothyroidism, such as weight gain,
hypotension, bradycardia, fatigue, depression, sensitivity to cold environments, hair loss, and dry skin.
Assess for signs of jaundice, and monitor liver enzymes. Assess for bleeding and blood dyscrasias, such as
agranulocytosis and jaundice. Clients should avoid children and pregnant women for one week after
administration of radioactive iodine (I-131) and limit close physical contact with others for a few days.
5. Glucocorticoid therapy for adrenocortical insufficiency: Assess vital signs for temperature and bloodpressure elevations. Monitor potassium, T3, T4, and glucose levels. Monitor clients on long-term
glucocorticoid therapy for osteoporosis and elevated serum cholesterol levels. Assess for signs and
symptoms of Cushing’s syndrome.
6. Antiadrenal therapy for adrenocortical insufficiency: Assess and monitor lab values, including platelet
count, bilirubin, hepatic-function tests, and prothrombin. Assess for jaundice, bruising, and bleeding.
Monitor client’s stress level, for orthostatic hypotension, and for dizziness and assist with ambulation.
Caution client to change positions slowly.
LEARNING OUTCOME 10
For each of the classes listed in Drugs at a Glance, know representative drugs, and explain the mechanisms of
drug action, primary actions, and important adverse effects.
Concepts
1. Anterior Pituitary Agents: Prototype drug: vasopressin injection (Pitressin). Mechanism of action: to
cause the renal collecting tubules to increase their permeability to water, thus enhancing water reabsorption.
Primary use: for treatment of diabetes insipidus. Adverse effects: hypertension; it can precipitate angina
episodes and myocardial infarction in clients with coronary artery disease. Excessive fluid retention can
cause water intoxication.
2. Thyroid Agents: Prototype drug: levothyroxine (Synthroid). Mechanisms of action: same as those of
thyroid hormone. Primary use: as the drug of choice for replacement therapy in clients with low thyroid
function. Adverse effects: hyperthyroidism, palpitations, dysrhythmias, anxiety, insomnia, weight loss, and
heat intolerance. Menstrual irregularities and osteoporosis can occur in women.
3. Antithyroid Agents: Prototype drug: propylthiouracil (PTU). Mechanism of action: to interfere with the
synthesis of T3 and T4 in the thyroid gland. It also prevents the conversion of T4 to T3 in the target tissues.
Primary use: for clients with hyperthyroidism. Adverse effects: symptoms of hypothyroidism. Rash and
transient leucopenia are the most common side effects. A small percentage of clients experience
agranulocytosis.
4. Adrenal Drugs—Glucocorticoids: Prototype drug: hydrocortisone (Aeroseb-HC, Alphaderm). Mechanism
of action: acts as a synthetic corticosteroid. Primary use: as the drug of choice for treating adrenocortical
insufficiency. Adverse effects: sodium and fluid retention; CNS effects, including insomnia, anxiety,
headache, vertigo, confusion, and depression. Hypertension, tachycardia, peptic ulcer disease, and
Cushing’s syndrome can also occur with long-term therapy.
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Prototype Drug

vasopressin injection (Pitressin)

levothyroxine (Synthroid)

propylthiouracil (PTU)

hydrocortisone (Aeroseb-HC, Alphaderm)
LEARNING OUTCOME 11
Use the nursing process to care for patients who are receiving drug therapy for pituitary, thyroid, and adrenal
disorders.
Concepts
1. Clients receiving pharmacotherapy with hypothalamic and pituitary hormones—Assessment: Obtain
a complete health history and a complete physical examination. Obtain a drug history including allergies,
current prescription and OTC drugs, herbal preparations, alcohol use or smoking. Be alert to possible drug
interactions. Evaluate appropriate laboratory findings (e.g., urine and serum osmolality, urine specific
gravity, serum protein, CBC, electrolytes, glucose, hepatic and renal function studies). Obtain baseline
height, weight, and vital signs. Obtain ECG if needed on patients taking growth hormone antagonists.
Assess for adverse effects: nausea, vomiting, diarrhea, headache.
2. Clients receiving pharmacotherapy with hypothalamic and pituitary hormones—Nursing diagnoses:
Deficient Fluid Volume; Diarrhea; Delayed Growth and Development; Situational Low Self-Esteem, related
to height, stature; Impaired Urinary Elimination (nocturnal enuresis); Deficient Knowledge (drug therapy).
3. Clients receiving pharmacotherapy with hypothalamic and pituitary hormones—Planning: The
client will experience therapeutic effects (e.g., height increase measurable over time, diuresis slows with
urine and serum osmolality within normal limits, return to normal bowel function, nocturnal enuresis has
stopped); be free from or experience minimal adverse effects. Verbalize an understanding of the drug’s
use, adverse effects, and required precautions. Demonstrate proper self- administration of the medication
(e.g., dose, timing, when to notify provider).
4. Clients receiving pharmacotherapy with hypothalamic and pituitary hormones—Implementation:
Patients taking growth hormone: Monitor height and weight at each clinical visit. Report lack of growth to
the health care provider. Patients taking growth hormone antagonists: Monitor levels of serum GH.
Monitor bowel sounds and decreases in diarrhea. Patients taking antidiuretic hormones: For patients with
diabetes insipidus, monitor urine output, urine and serum osmolality, and urine specific gravity for return
to normal limits. Monitor for any complaints of muscle, joint or bone pain, particularly in the knee or hip,
or any changes in gait. Monitor glucose levels, particularly in diabetic patients. Report consistent
elevations to the health care provider. Monitor vital signs, especially pulse and blood pressure for patients
with cardiac disease Monitor daily weight, output, lung sounds, and for peripheral edema. Monitor for
signs of peripheral ischemia, or angina and report immediately. Monitor nutritional and fluid intake
instruct patient or care giver in proper self-administration of drug (e.g., during evening meal).
5. Clients receiving pharmacotherapy with hypothalamic and pituitary hormones—Evaluation: The
client will experience height increase measurable over time, diuresis slows with urine and serum
osmolality within normal limits, return to normal bowel function, nocturnal enuresis has stopped; be free
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from or experience minimal adverse effects. Verbalize an understanding of the drug’s use, adverse effects,
and required precautions. Demonstrate proper self-administration of the medication (e.g., dose, timing,
when to notify provider).
6. Clients receiving thyroid replacement and antithyroid drugs— Assessment: Obtain a complete health
history including cardiovascular, gastrointestinal, hepatic, renal disease, pregnancy or breast-feeding.
Obtain a drug history including allergies, current prescription and OTC drugs, herbal preparations, alcohol
use or smoking. Be alert to possible drug interactions. Assess for the presence and history of symptoms of
hypothyroidism. Evaluate appropriate laboratory findings (e.g., T3, T4, and TSH levels, CBC, platelets,
electrolytes, glucose, and lipid levels). Obtain baseline height, weight, and vital signs. Obtain ECG as
needed. Assess for adverse effects: Hypotension or hypertension, tachycardia, especially associated with
angina should be reported immediately.
7. Clients receiving thyroid replacement and antithyroid drugs—Nursing diagnoses: Activity
Intolerance; Fatigue; Constipation; Deficient Knowledge (drug therapy); Risk for Infection related to
adverse drug effects.
8. Clients receiving thyroid replacement and antithyroid drugs—Planning: The client will experience
therapeutic effects (e.g., decrease in symptoms, thyroid lab studies return to within normal limits); be free
from or experience minimal adverse effects. Verbalize an understanding of the drug’s use, adverse effects,
and required precautions. Demonstrate proper self-administration of the medication (e.g., dose, timing,
when to notify provider).
9. Clients receiving thyroid replacement and antithyroid drugs— Implementation: Monitor vital signs—
appetite, weight, sensitivity to heat or cold, sleep patterns, and ADLs for return to normal limits. Monitor
for decreasing symptoms related to hypothyroidism and to hyperthyroidism. Monitor T3, T4, and TSH
levels. Avoid iodine-containing foods. Monitor for signs of infection: fever, rashes, sore throat, malaise,
fatigue or weakness. Monitor CBC and platelet counts. Monitor blood-glucose levels, especially in
individuals with diabetes mellitus. Ensure patient safety, especially in the elderly. Observe for dizziness
and monitor ambulation until effects of drug are known. Ensure patient and care giver safety if radioactive
iodine is used. Instruct the patient and/or family in proper self-administration of drug (e.g., take the drug in
the morning at the same time each day).
10. Clients receiving thyroid replacement and antithyroid drugs—Evaluation: The client will experience a
decrease in symptoms; thyroid lab studies return to within normal limits. The client will be free from or
experience minimal adverse effects. Verbalize an understanding of the drug’s use, adverse effects, and
required precautions. Demonstrate proper self-administration of the medication (e.g., dose, timing, when to
notify provider).
11. Clients receiving systemic glucocorticoid therapy— Assessment: Obtain a complete health history and a
complete physical examination. Determine the reason the medication is being administered. Evaluate
appropriate laboratory findings (e.g., CBC, platelets, electrolytes, glucose, lipid profile, hepatic or renal
function studies). Obtain baseline vital signs and weight. Assess for and promptly report adverse effects.
12. Clients receiving systemic glucocorticoid therapy—Nursing diagnoses: Deficient Knowledge (drug
therapy); Risk for Fluid Volume Excess related to fluid retention properties of glucocorticoids; Risk for
Injury related to adverse drug effects; Risk for Infections related to adverse drug effects; Risk for Impaired
Skin Integrity related to adverse drug effects.
13. Clients receiving systemic glucocorticoid therapy—Planning: The client will experience therapeutic
effects (e.g., decreased signs and symptoms of inflammation or allergic response); be free from or
experience minimal adverse effects. Verbalize an understanding of the drug’s use, adverse effects and
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required precautions. Demonstrate proper self-administration of the medication (e.g., dose, timing, when to
notify provider).
14. Clients receiving systemic glucocorticoid therapy— Implementation: Monitor vital signs, especially
blood pressure and pulse. Report tachycardia or BP over 140/90. Monitor for abdominal pain, black or
tarry stools, blood in the stool, hematemesis or coffee-ground emesis, dizziness, hypotension, especially if
associated with tachycardia. Monitor for infection. Protect the client from potential infections. Monitor the
client’s compliance with drug regimen. Monitor for symptoms of Cushing’s syndrome. Monitor bloodglucose levels. Monitor skin and mucous membranes for lacerations, abrasions, or break in integrity.
Monitor GI status for peptic ulcer development. Monitor serum electrolytes. Monitor for osteoporosis (e.g.,
bone density testing) periodically in patients on long-term corticosteroids. Encourage adequate calcium
intake, avoidance of carbonated sodas, and weight-bearing exercise. Monitor changes in musculoskeletal
system. Monitor emotional stability. Weigh the patient daily and report weight gain or increasing
peripheral edema. Measure intake and output in the hospitalized patient. Monitor vision periodically in
patients on corticosteroids. Do not stop the drug abruptly. The drug must be tapered off if used longer than
1 or 2 weeks. Instruct the patient and/or family in proper self-administration of drug (e.g., with food or
milk).
15. Clients receiving systemic glucocorticoid therapy—Evaluation: The client will experience decreased
signs and symptoms of inflammation or allergic response; be free from or experience minimal adverse
effects. Verbalize an understanding of the drug’s use, adverse effects, and required precautions.
Demonstrate proper self-administration of the medication (e.g., dose, timing, when to notify provider).
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