healthcare

1. 1
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NCM-116
Assessment and Management of Patients with Endocrine Disorders (Part-2)
Topic Outline
1. Cushing Syndrome
2. Addison’s Disease
3. Pheochromocytoma
4. Diabetes Insipidus (DI)
5. Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Learning Objectives
After studying this topic, you will be able to:
 Compare Addison’s disease with Cushing syndrome; Diabetes Insipidus (DI) and Syndrome of
Inappropriate Antidiuretic Hormone (SIADH): their causes, clinical manifestations, management, and
nursing interventions.
 Discuss common disorders of the adrenal glands, incorporating pathophysiology, manifestations, and
associated nursing care.
 Use the nursing process as a framework for care of patients with Cushing syndrome and Addison’s
disease; Pheochromocytoma; Diabetes Insipidus and Syndrome of Inappropriate Antidiuretic
Hormone.
 Compare and contrast common disorders of the pituitary gland and the resulting manifestations.
Introduction
Disorders of the adrenal cortex or adrenal medulla result in changes in the production of
adrenocorticotropic hormone (ACTH). Hormones of the adrenal cortex are essential to life and maintain
homeostasis in response to stressors. Disorders of the adrenal cortex result in complex physical, psychological,
and metabolic alterations. While the pituitary gland produces hormones that affect multiple body systems through
the regulation of endocrine function. Target tissues include the thyroid, adrenal cortex, ovary, uterus, mammary
glands, testes, and kidneys. Disorders result from an excess or deficiency of one or more of the pituitary hormones
due to a pathological condition within the gland itself or to hypothalamic dysfunction. Although disorders of the
pituitary cause diverse and serious problems, they are not as common as disorders of other endocrine glands.
Nursing care of patients with endocrine disorders is directed towards meeting physiological needs,
providing education, and ensuring psychological support for the person and family.
Pre-lecture Quiz
True or False: Write T if the statement is True and F if the statement is False
1. The major function of the adrenocortical hormone is the regulation of serum glucose and sodium.
2. Cushing syndrome is a group of symptoms produced by an over secretion of adrenocorticotropic hormone;
characterized by truncal obesity, “moon face,” abdominal striae, and hypertension
3. Hypertension, hypermetabolism, and hyperglycemia are clinical manifestations of Diabetes Insipidus
4. Acromegaly is characterized by progressive enlargement of peripheral body parts resulting from excessive
secretion of growth hormone
5. Hypophysectomy is the removal or destruction of all or part of the pituitary gland
Fill-in-the-Blank. Read each statement carefully then write the best response on the space provided.
1. The major action of the ____________ is controlling the release of pituitary hormones.
2. Over secretion of the anterior pituitary gland most commonly involves ACTH or growth hormone and
results in ____________ syndrome or acromegaly.
3. ___________ antidiuretic hormone secreted by the posterior pituitary
4. ___________ is a condition in which abnormally large volumes of dilute urine are excreted as a result of
deficient production of vasopressin
5. _____________ disease occurs when the adrenal cortex function is inadequate to meet the patient’s need
for cortical hormones.
Key
Answer
to
Pre-assessment:
T/F:
1.
True;
2.
True;
3.
False;
4.
True;
5.
True
Fill-in-the-Blank:
1.
Hypothalamus;
2.
Cushing;
3.
Vasopressin;
4.
Diabetes
Insipidus;
5.
Addison

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NCM-116
ENDOCRINE AND METABOLIC SYSTEM
ADRENAL GLANDS: are located on top of each kidney (suprarenal glands).
It consists of two parts:
1. Adrenal Medulla: the inner portion of the adrenal
gland, is not necessary to maintain life but enables a
person to cope with stress. It is part of the
sympathetic nervous system, releases two potent
hormones called epinephrine and norepinephrine. The
hypothalamus controls the secretion of these two
catecholamines. Both produce effects on the body
similar to those produced by activation of the sympathetic nervous system. For these reasons epinephrine
and norepinephrine are called “sympathomimetic agents.” During Stressful situation:
 Epinephrine (adrenalin) acts on alpha and beta receptors to increases heart rate and force of
contraction leading to increased cardiac output, increases conversion of glycogen to glucose in the
liver, dilates bronchioles, decrease peristalsis, causes vasodilation in skeletal muscles and brain,
causes vasoconstriction in skin and viscera, increases the use of fats for energy, and increases the
rate of cell respiration/metabolism.
 Norepinephrine (noradrenaline) acts primarily on alpha receptors to produce peripheral vascular
constriction or resistance thereby causing a marked rise in blood pressure.
2. Adrenal Cortex: the outer portion of the gland, is essential to life and for survival. It releases 3 types of
adrenocortical hormones called “Corticosteroids.” One group regulates sodium and potassium balance,
the second regulates carbohydrate, fat, and protein metabolism; and the third is linked with sexual
characteristics.
 Mineralocorticoids
o Aldosterone is the most abundant mineralocorticoids. The target organs of aldosterone are
the kidneys. It increases the reabsorption and retention of sodium, secondary water retention,
and excretion of potassium by the kidney. Thereby it primarily functions to conserve sodium
and maintain extracellular fluid (ECF) volume. These help to sustain normal BP and cardiac
output.
 Glucocorticoids: regulates blood glucose level.
o Cortisol is the principal glucocorticoid. Increases use of fats and excess amino acids
(gluconeogenesis) for energy, which raises the blood glucose level by the liver (antagonize
action of insulin); decreases use of glucose for energy (except for the brain), increases
conversion of glucose to glycogen in the liver, enhance protein catabolism and amino acids
are transported into the ECF and then to the liver, where they are converted to glucose
(excessive secretion of the glucocorticoids causes tissue wasting); sodium retention,
secondary water retention, and potassium excretion all increase (overabundance of
glucocorticoid secretion results in hypervolemia and hypertension owing to sodium and water
retention); anti-inflammatory effect by blocking the effects of histamine and stabilizes
lysosomal membrane, preventing excessive tissue destruction; decrease immunity since too
much glucocorticoids impedes healing, decrease antibody formation, lowers the number of
circulating eosinophils and lymphocytes, and lowers the resistance of infection; increase
resistance to stress if secreted in sufficient amount that enables the individual to cope with
stress effectively, provided the stress is not overwhelming (insufficient production of
glucocorticoids decreases resistance to stress.
 Sex Hormone [(Adrenosterones (adrenal androgens)]. It secretes very small quantities of androgens
(masculinizing hormone) and even smaller quantities of estrogen (female sex hormone).
CUSHING’S SYNDROME
A syndrome involving excessive production of adrenocortical hormones, primarily cortisol but also androgens
and mineralocorticoids.
Etiology
 Pituitary Cushing syndrome (Cushing disease): hyperplasia of the adrenal cortex due to overproduction
of ACTH, usually from a pituitary adenoma or hyperplasia.
 Adrenal Cushing syndrome: tumor of the adrenal cortex.

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NCM-116
Pathophysiology: The normal feedback mechanisms that control adrenocortical function are ineffective, resulting
in secretion of adrenal cortical hormone despite adequate amounts of these hormones in the circulation. The
manifestations of Cushing’s syndrome are the result of excess hormones.
Clinical Manifestations
A. Manifestation due to excess Glucocorticoids.
1. Persistent hyperglycemia, which may result in the development of diabetes mellitus.
2. Protein tissue wasting and excessive deamination of amino acids, which results in (a) stunting of linear
growth in children (b) weakness due to muscle wasting, (c) skin fragility & capillary fragility resulting in
ecchymosis, and (d) osteoporosis due to bone matrix wasting → hypercalcemia → hypercalciuria
3. Abnormal fat distribution (in conjunction with edema), which results in moon face (round face), Buffalo
hump (supraclavicular fat pad on the person’s neck), and truncal obesity (weight gain) with slender/thin
limbs; striae on the trunk.
4. Increase susceptibility to infection and poor wound healing
5. Emotional/mental changes including mood swings, euphoria, and depression.
B. Manifestation due to excess Mineralocorticoids
1. Hypernatremia & Hypokalemia→ muscle weakness & cardiac arrhythmia
↓
2. Fluid (H2O) retention → oliguria
↓
3. Hypervolemia → Hypertension & congestive heart failure
↓
4. Edema → Weight gain
C. Manifestation due to excess Sex hormone
1. Women experience virilism (masculinization) may occur as a result of excessive androgens.
a. Hirsutism—excessive growth of hair on the face and midline of the trunk.
b. Breasts—atrophy.
c. Clitoris—enlargement.
d. Voice—masculine.
e. Loss of libido.
f. If exposed in utero—possible hermaphrodite.
2. Males—loss of libido.
Diagnostic Test
1. Hyperglycemia and hypokalemia
2. Depressed eosinophil and lymphocyte counts
3. Elevated plasma cortisol and 24-hour urine cortisol results
4. Elevated ACTH in patients with pituitary tumors
Surgical Management and Radiation
1. Adrenalectomy for adrenal tumors/hyperplasia
2. Transsphenoidal hypophysectomy (pituitary removal) for pituitary gland tumor
3. Radiation therapy
Medical Management: cortisol synthesis–inhibiting medications
1. Mitotane (Lysodren): an agent toxic to the adrenal cortex that inhibits the production of glucocorticoids
by the adrenal gland.
2. Metyrapone (Metopirone): decrease cortisol production in patients who do not respond to mitotane therapy
3. Aminoglutethimide (Cytadren): blocks cortisol production.
Nursing Diagnoses
1. Impaired skin integrity related to altered healing, thin and fragile skin, and edema.
2. Dressing, grooming, toileting self-care deficit related to muscle wasting, osteoporosis, weakness, and
fatigue.
3. Disturbed body image related to altered physical appearance and emotional instability.
Nursing Interventions (preoperative)
1. Maintaining skin integrity
a. Assess skin frequently to detect reddened areas, breakdown or tearing of skin, excoriation,
infection, or edema.

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NCM-116
b. Handle skin and extremities gently to prevent trauma; protect from falls by use of side rails.
c. Avoid the use of adhesive tape to reduce the risk of trauma to the skin on its removal.
d. Encourage patient to turn in bed frequently or to ambulate to reduce pressure on bony
prominences and areas of edema.
e. Provide foods low in sodium to minimize edema formation.
f. Assess intake and output and daily weight to evaluate fluid retention.
2. Encouraging active participation in self-care
a. Assist patient with ambulation and hygiene when weak and fatigued due to muscle wasting and
hypokalemia
b. Assist patient in planning schedule to permit exercise and encourage to rest when fatigued.
c. Encourage gradual resumption of activities as the patient gains strength.
d. Instruct patient correct body mechanics to avoid pain or injury during activities.
e. Protect patient from accident and use assistive devices during ambulation to prevent falls and
fractures.
f. Encourage foods high in potassium (bananas, orange juice, tomatoes), and administer potassium
supplement, as prescribed, to counteract weakness related to hypokalemia.
3. Strengthening body image
a. Encourage the patient to verbalize concerns about illness, changes in appearance, and altered role
functions.
b. Be alert for evidence of depression; this may progress to suicide; alert health care provider of
mood changes, sleep disturbance, change in activity level, change in appetite, or loss of interest
in visitors or other experiences.
c. Refer for counseling, if indicated.
d. Explain to the patient who has benign adenoma or hyperplasia that, with proper treatment,
evidence of masculinization can be reversed.
4. Other nursing management
a. Diet: provide low-calorie, low-carbohydrate, low-fat, and low-sodium, but with ample amount of
protein, potassium, and calcium content (dairy products, broccoli).
b. Assess the person carefully for signs of severe hypertension.
c. Protect people with Cushing’s syndrome from exposure to an infectious organism.
Postoperative Care
1. Observe for signs of shock
2. Measure urine hourly and observe for oliguria
3. Monitor closely for infection because glucocorticoid administration interferes with immune function;
maintain sterile technique, clean environment, and good handwashing.
4. Monitor thyroid function tests and provide HRT, as ordered, after hypophysectomy.
5. Encourage coughing, turning, and deep breathing to prevent dangerous respiratory infection.
6. Monitor fluid intake and output and urine-specific gravity to detect DI caused by ADH deficiency after
hypophysectomy.
ADDISON’S DISEASE (Adrenocortical Insufficiency)
Hyposecretion of adrenal cortex hormone
Etiology
 Primary adrenocortical insufficiency (Addison disease)—destruction and subsequent hypofunction of the
adrenal cortex, usually caused by an autoimmune process.
 Secondary adrenocortical insufficiency—ACTH deficiency from pituitary disease or suppression of
hypothalamic-pituitary axis by corticosteroid treatment for nonendocrine disorders causes atrophy of the
adrenal cortex.
Pathophysiology
 Aldosterone deficiency causes numerous fluid and electrolyte imbalances. A deficiency causes increased
sodium excretion, which results in the following chain of events: (a) water excretion increases, (b) ECF
volume becomes depleted, (c) hypotension develops, (d) cardiac output decreases, and (e) heart becomes
smaller owing to its diminished workload. Second, excessive potassium level results in arrhythmia.
 Glucocorticoid deficiency, gluconeogenesis decrease, with resultant hypoglycemia and liver glycogen
deficiency. The person grows weak and exhausted and suffers from anorexia, weight loss, nausea, and
vomiting. An emotional disturbance may develop. Glucocorticoid deficiency diminishes resistance to
stress. Finally, cortisol deficiency results in a failure to inhibit anterior pituitary secretion of ACTH and

5. 5
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NCM-116
melanocyte-stimulating hormone (MSH). MSH stimulates the epidermal melanocytes, which manufacture
melanin, a dark pigment. Which results in increase pigmentation of the skin and mucous membrane.
 Androgen deficiency, women with Addison’s disease have less axillary and pubic hair growth.
Clinical Manifestations
A. Manifestation due to deficient Glucocorticoids.
1. Hypoglycemia and low basal metabolic rate → muscular Weakness and fatigability
2. Emotional/mental changes like depression, irritability, and anxiety apprehension caused by hypoglycemia
and hypovolemia.
3. Ineffective ability to cope with stress.
4. Hyperpigmentation: bronzed pigmentation of the skin (eternal tan).
B. Manifestation due to deficient Mineralocorticoids
1. Hyponatremia & hyperkalemia → cardiac arrhythmia
↓
2. Fluid loss (H2O) → polyuria
↓
3. Hypovolemia → hypotension
↓
4. Dehydration → weight loss
5. G.I. problems like anorexia, nausea, vomiting, diarrhea & abdominal pain due to hyperkalemia
C. Manifestation due to deficient Sex hormone
1. Female: less axillary & pubic hair
2. Male: impotence
Diagnostic Evaluation (Blood studies)
1. Hypoglycemia, hyponatremia and hyperkalemia
2. Low fasting plasma cortisol, and low aldosterone levels
Medical Management (Replacement therapy)
1. Cortisone (Cortone), prednisone (Deltasone), hydrocortisone (Solu-Cortef). Hydrocortisone is usually the
drug of choice for adrenocortical replacement because it has both glucocorticoids and mineralocorticoid
properties.
2. Fludrocortisone (Florinef) for mineralocorticoid deficiency. Administer after a meal or with an antacid to
lessen gastric irritation and the possible development of a peptic ulcer.
Nursing Diagnoses
1. Deficient Fluid Volume related to renal losses of sodium and water.
2. Risk for Infection related to ineffective stress response.
3. Activity Intolerance related to decreased cortisol production and fatigue.
Nursing Management
1. Achieving normal fluid and electrolyte balance
a. Assess fluid intake and output and serial daily weights.
b. Monitor vital signs frequently; a drop in BP may suggest an impending crisis.
c. Monitor results of serum sodium and potassium.
d. Assess skin turgor and mucous membranes for dehydration.
e. Encourage diet high in sodium and fluid content but low potassium.
f. Administer or teach self-administration of prescribed glucocorticoids and mineralocorticoids
g. Administer IV infusions of sodium, water, and glucose, as indicated.
2. Protecting Well-Being
a. Minimize stressful situations.
b. Protect patient from infection.
i. Control patient’s contacts so that infectious organisms are not transmitted.
ii. Protect patient from drafts, dampness, exposure to cold.
iii. Prevent overexertion.
iv. Use meticulous handwashing and sterile techniques.
c. Assess the comfort and emotional status of the patient.
i. Control the temperature of the room to avoid sharp deviations in the patient’s
temperature.
ii. Maintain a quiet, peaceful environment; avoid loud talking and noisy radios.

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NCM-116
d. Observe and report early signs of Addisonian crisis (sudden drop in BP, nausea & vomiting, fever).
3. Increasing Activity Tolerance
a. Assist the patient with ADLs.
b. Provide periods of rest and activity to avoid overexertion.
c. Provide for a high-calorie, high-protein diet.
4. Observe for early signs of Addisonian Crisis (Acute adrenal insufficiency). It may be precipitated by
physiologic stress, such as surgery, infection, trauma, dehydration.
a. Clinical Manifestations
i. Extreme weakness
ii. Hyperpyrexia
iii. Severe hypotension and hypovolemia → vascular collapse → shock → coma and death.
b. Intervention
i. Intravenous administration of sodium chloride solution to replace sodium ions and glucose
administration to correct hypoglycemia
ii. Hydrocortisone/IV, then oral
iii. Vasopressors such as epinephrine
Patient Education
1. Inform the client that the therapy must be continued throughout life and not to discontinue abruptly
because doing so may cause severe withdrawal symptoms, Addisonian crisis leading to possible shock and
death.
2. Emphasize the importance of taking more hormones when under stress.
3. The patient & family need to know the signs of excessive & insufficient hormone replacement
PHEOCHROMOCYTOMA
A catecholamine-secreting neoplasm associated with hyperfunction of the adrenal medulla.
Incidence: most common between the ages of 40 and 50
Pathophysiology
Increase epinephrine and norepinephrine secretion
↓
Sympathetic nervous system overactivity
↓
5 H’s (hypertension, headache, hyperhidrosis, hypermetabolism, hyperglycemia)
Clinical Manifestations
1. Hypertension may be intermittent) or persistent → headaches and vision disturbances. The chronic form
mimics essential hypertension; however, antihypertensives are not effective.
2. Hypermetabolism →excessive perspiration, tremor, face flushing, and nervousness or anxiety
3. Hyperglycemia (conversion of liver and muscle glycogen to glucose due to epinephrine secretion)
Diagnostic Evaluation
1. Vanillylmandelic Acid Test (VMA test) to detect excess epinephrine and norepinephrine. Vanillylmandelic
acid is a metabolite of epinephrine.
 24-hour urine specimen
 (+) an elevated level of VMA
2. Catecholamines (epinephrine and norepinephrine) metanephrine (MN), a catecholamine metabolite, in
urine and blood are elevated are the most direct and conclusive tests for overactivity of the adrenal
medulla.
3. CT scan and magnetic resonance imaging (MRI) of the adrenal glands or the entire abdomen are done to
identify a tumor.
Medical Management
1. Anti-hypertensive drugs
a. Alpha-adrenergic blockers, such as phentolamine or phenoxybenzamine, inhibit the effects of
catecholamines on BP. Selective alpha1-adrenergic blocker with fewer side effects, such as
prazosin (Minipress), terazosin (Hytrin), or doxazosin (Cardura)
b. Beta-blockers such as propranolol (Inderal)
c. Calcium channel blockers such as nifedipine (Procardia) and nicardipine (Cardene)
2. Administer sedatives, as prescribed, to promote relaxation and rest.

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NCM-116
Surgical management: Adrenalectomy (unilateral or bilateral)
Nursing Diagnoses
1. Anxiety related to the systemic effects of epinephrine and norepinephrine.
2. Ineffective Tissue Perfusion related to hypotension during the postoperative period.
Nursing Management
1. Reducing Anxiety
a. Remain with the patient during acute episodes of hypertension. Hypertensive crisis may result in
complications such as CVA, cardiac dysrhythmias, and myocardial infarction.
b. Ensure bed rest and elevate the head of bed 45 degrees elevated during severe hypertension.
c. Carry out tasks and procedures in a calm, unhurried manner when with the patient.
d. Instruct patient about the use of relaxation exercises.
e. Reduce environmental stressors by providing a calm, quiet environment. Restrict visitors.
f. Eliminate stimulants (coffee, tea, cola) from the diet and smoking.
g. Reduce events that precipitate episodes of severe hypertension like palpation of the tumor,
physical exertion, emotional upset.
h. Prepare patient for adrenalectomy
2. Maintaining Tissue Perfusion Postoperatively
a. Monitor vital signs, ECG, arterial BP, neurologic status, and urine output closely postoperatively.
b. Assess for and report complications of hypertension, hypotension, and hyperglycemia.
c. Maintain adequate hydration with IV infusion to prevent hypotension. (Because reduction of
catecholamines immediately postoperatively causes vasodilation and enlargement of vascular
space, hypotension may occur.)
d. Monitor intake and output and laboratory results for BUN, creatinine, and glucose levels.
PITUITARY GLAND (HYPOPHYSIS)
Located at the inferior aspect of the brain that hangs from the hypothalamus and is enclosed within the
Sella turcica of the sphenoid bone at the base of the brain. Its function is regulated by the hypothalamus. The
pituitary consists of two parts that are structurally and functionally separate: the anterior pituitary and the
posterior pituitary. Hypothalamic control of the anterior pituitary is mediated by releasing factors secreted by the
hypothalamus; the posterior pituitary is regulated through direct neural stimulation.

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NCM-116
1. Anterior Pituitary (adenohypophysis)
a. Growth hormone (somatotropin): affects the growth of body tissues, bones, and muscles
o Hypersecretion
 Children: Gigantism (before the closure of the epiphyseal plates). It is characterized
by exaggerated growth and height.
 Adult: Acromegaly (after the closure of the epiphyseal plates). Primarily caused by a
pituitary tumor. It is characterized by thickening and protrusion the jaw and other
facial bones become disproportionately large; broadening of the bones of the hands
and feet; organomegaly
o Hyposecretion: Dwarfism that is characterized by failure to grow in height.
b. Prolactin: affects mammary glands to stimulate milk production (lactation).
o Hypersecretion: Galactorrhea (excessive milk production)
o Hyposecretion: Absence of milk during lactation
c. ACTH (Adrenocorticotropic Hormone): stimulates the adrenal cortex to produces steroids
o Hypersecretion: Secondary Cushing’s Disorder
o Hyposecretion: Secondary Addison’s Disorder
d. TSH (Thyroid-Stimulating Hormone): stimulates the thyroid gland to produce a hormone
o Hypersecretion: Secondary Hyperthyroidism
o Hyposecretion: Secondary Hypothyroidism
e. Gonadotropin (Follicle-stimulating Hormone & Luteinizing Hormone): affects growth, maturity,
and functioning of primary and secondary sex characteristics
o Hypersecretion: Precocious Puberty
o Hyposecretion: failure to develop secondary sex characteristics that normally develop at the
age of puberty
Males: Females:
Small phallus and testicles Failure to develop breast
NO growth of body hair No growth of body hair
 libido No ovulation
Impotence No menstruation
Aspermia Infertility
f. MSH (Melanocyte – Stimulating Hormone): stimulates adrenal cortex; affects pigmentation
o Hypersecretion: hyperpigmentation of the skin (“eternal tan” or bronze appearance of the
skin)
o Hyposecretion: hypopigmentation of the skin (Albinism)
2. Posterior Pituitary Gland (Neurohypophysis): stores and releases hormone synthesized in the
hypothalamus.
a. ADH (Antidiuretic Hormone, Vasopressin): increases water reabsorption by the kidneys that result
in decrease urinary output and increase blood volume.
o Hypersecretion: SIADH (Syndrome of Inappropriate Antidiuretic hormone) characterized by
excessive retention of water by the renal tubules.
o Hyposecretion: DI (Diabetes Insipidus) is characterized by the inability of the kidney tubules
to retain water.
b. Oxytocin: stimulates contraction of myometrium of the uterus during labor and release of milk
from mammary glands.
DIABETES INSIPIDUS
A disorder of water metabolism caused by deficiency of antidiuretic hormone (ADH, vasopressin) secreted by
the posterior pituitary gland. It is characterized by the inability of the kidney tubules to retain water.
Etiology
1. Primary: idiopathic
2. Secondary: head trauma, neurosurgery, tumors, vascular accident (infarct), infection (meningitis,
encephalitis).
3. Nephrogenic DI (failure of the renal tubules to respond to ADH)
4. Certain drugs that interfere with ADH synthesis or secretion (e.g. lithium carbonate, demeclocycline)

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NCM-116
Pathophysiology
ADH deficiency
↓
Inability of the kidney to retain or reabsorb water
↓
Polyuria → Inappropriately diluted urine
↓
Severe dehydration
Clinical Manifestations
1. Marked polyuria with a daily output of greater than 6-20 liters of very diluted urine, with urine specific
gravity of 1.001 – 1.005 (Normal: 1.010- 1.025).
2. Polydipsia (intense thirst); 2-20 liters of fluid daily and patient has craving for cold water
3. Dehydration → weight loss
4. Hypovolemia → hypotension
5. Hypernatremia
Diagnostic Evaluation
1. Patient’s history and clinical manifestations of polyuria and polydipsia
2. Increase (high) blood or serum osmolality (hemoconcentration); Decrease (low) urine specific gravity or
osmolality
3. Water deprivation test
a. Instruct the person not to drink for 8-12 hours, in an effort to concentrate the urine.
b. (+) if the urine remains diluted.
4. Decreased to absent serum and urine ADH.
5. Elevated serum sodium level (hypernatremia)
Medical Management
1. Administration of ADH or its derivatives.
a. Desmopressin acetate (DDAVP): a synthetic vasopressin derivative administered intranasally; the
patient sprays the solution into the nose through a flexible calibrated plastic tube. One or two
administrations daily to control the symptoms. Duration of action 8 to 12 hours.
b. Chlorpropamide (Diabinese): potentiates the action of vasopressin on the renal concentrating
mechanism.
2. For patients with nephrogenic DI, chlorpropamide or thiazide diuretics may be of value. Reversible by
discontinuing causative medication if the cause is drug-related.
Nursing Diagnosis: Risk for Deficient Fluid Volume related to the disease process.
Nursing Management
1. Maintaining adequate fluid volume
a. Measure fluid intake and output accurately.
b. Obtain daily weights.
c. Monitor hemodynamic status, as indicated, via frequent BP, heart rate, central venous pressure,
and other measurements.
d. Maintain adequate fluid intake and administer IV fluids as indicated.
e. Administer or teach self-administration of medication, as prescribed, and document patient
response.
Patient Education
1. Advise patient to avoid limiting fluid to decrease urinary output.
2. Teach patient to be alert for signs of dehydration—decreased weight, decreased urine output, increased
thirst, dry skin, and mucous membranes; and overhydration—increased weight and edema; report these
to the health care provider.
3. Eliminate coffee & tea from the diet – may have an exaggerated diuretic effect.
4. Lifelong hormone replacement. Have the patient demonstrate intranasal and injection technique.
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH)
Over secretion of ADH from the pituitary gland and resulting in excess water conservation.

10. 10
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NCM-116
Etiology
 Bronchogenic carcinoma in which malignant lung cells synthesize and release ADH (nonendocrine origin)
 Central nervous system disorders such as head injury, brain surgery or tumor, and infection, are thought
to produce SIADH by direct stimulation of the pituitary gland.
 Pharmacologic agent (e.g., vincristine [Oncovin], phenothiazines, tricyclic antidepressants, thiazide
diuretics); nicotine and overuse of vasopressin therapy
Pathophysiology
Over /excessive secretion of ADH
↓
Excessive water retention
↓
Oliguria
↓
Fluid overload
Clinical Manifestations
1. Oliguria (decreased urine output) with increase urine specific gravity or osmolarity (concentrated)
2. Weight gain, edema
3. Hypervolemia → Hypertension
4. Dilutional hyponatremia
5. Altered mental status (e.g., HA, confusion, lethargy, seizure) and coma in severe hyponatremia.
Diagnostic Evaluation
1. Decrease (low) blood or serum osmolality (hemodilution); Increase (high) urine specific gravity or
osmolality
2. Increase level of serum ADH
3. Low serum sodium level (hyponatremia)
Medical Management
1. Diuretics as prescribed
2. Declomycin (Demeclocycline) as prescribed. It inhibits ADH-induce water reabsorption & produces diuresis
3. Anti-HPN
Nursing Diagnosis: Risk for fluid volume excess
Nursing Management
1. Preventing fluid volume excess
a. Restrict fluid intake as indicated
b. Monitor I & O, daily weight, electrolyte level
c. Regularly assess V/S, cardiac and mental status
Comparison of posterior pituitary gland disorders
SIADH DIABETES INSIPIDUS
Excessive ADH Deficient ADH
Fluid volume excess Fluid volume deficit
Restrict fluid intake Encourage fluid intake
Demeclocycline (Declomycin) (oral agent)
causes excessive urination
Desmopressin (DDA VP) (nasal spray) causes
increased water reabsorption
Activity
Written Assignments: 1. Differentiate between hyperparathyroidism and hypoparathyroidism. Complete
a short-written summary of education to provide to a patient for self-care at home; 2. Using the nursing process
as a framework, prepare a care plan for a patient with Cushing syndrome.
Group Assignment: Addison disease and Cushing syndrome are both adrenal disorders. As a group,
compare their causes, clinical manifestations, management, and nursing interventions.
Web Assignment: Research the Internet to find therapeutic uses of corticosteroid therapy. Summarize
your findings

11. 11
All information contained in this module are property of UCU and provided solely for educational purposes. Reproduction, storing in a retrieval system, distributing, uploading or posting online, or transmitting
in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise of any part of this document, without the prior written permission of UCU, is strictly prohibited.
NCM-116
Interactive Link
https://tinyurl.com/576e45vu (Cushing’s Disease vs. Addison’s Disease)
https://tinyurl.com/4yrdes9f (Pheochromocytoma)
https://tinyurl.com/28khaunm (SIADH vs. DI)
Summary
The adrenal glands regulate energy and fluid balance through corticosteroids and mineralocorticoids.
Cushing’s and Addison’s diseases are opposites and treatment eliminates the signs and symptoms of one and
creates the manifestations of the other. People with these disorders require education until they fully grasp the
significance of the condition and the importance of adhering to the treatment plan.
The pituitary gland, in conjunction with the hypothalamus, is the master gland of the body. Fifteen
hormones and regulatory factors are synthesized in the anterior pituitary and hypothalamus; many are trophic
hormones that stimulate the release of other hormones.
Case Study: Cushing Syndrome
Patient Profile: Tom is a 29-year-old high school teacher. He seeks the advice of his health care provider because
of changes in his appearance over the past year.
Subjective Data
 Reports weight gain (particularly through his midsection), easy bruising, and edema of his feet, lower
legs, and hands
 Has been having increasing weakness and insomnia
Objective Data
 Physical examination: BP 150/110; 2+ edema of lower extremities; purplish striae on abdomen; thin
extremities with thin, friable skin; severe acne of the face and neck
 Blood analysis: Glucose 167 mg/dL; white blood cell (WBC) count 13,600/mm3
; lymphocytes 12%;
red blood cell (RBC) count 6.6 million/mm3
; K+
3.2 mEq/L
Critical Thinking & Discussion Questions
Using a separate sheet of paper, answer the following questions:
1. Discuss the probable causes of the alterations in Tom’s laboratory results.
2. Explain the pathophysiology of Cushing syndrome.
3. What diagnostic testing would identify the cause of Tom’s Cushing syndrome?
4. What is the usual treatment of Cushing syndrome?
5. What is meant by a “medical adrenalectomy”?
6. Priority Decision: What are the priority nursing responsibilities in the care of this patient?
7. Priority Decision: Based on the assessment data presented, what are the priority nursing diagnoses? Are
there any collaborative problems?
Readings and References
 Smeltzer, Suzanne C. (2014). Brunner & Suddarth’s. Textbook of Medical-Surgical Nursing-13th Edition,
Wolters Kluwer/Lippincott Williams & Wilkins
 Lemone et al. (2017). Medical-Surgical Nursing Critical Thinking for Person-Centered Care, 3rd Edition,
Pearson Australia.
 Nettina, Sandra N. (2019). Lippincott Manual of Nursing Practice, 11th Edition, Wolters Kluwer.
 Lewis et al. (2014). Medical-Surgical Nursing Assessment and management of Clinical Problems, 9th
Edition. Mosby, an imprint of Elsevier Inc.
 Udan (2017). Medical-Surgical Nursing Concepts and Clinical Applications, 3rd edition, APD Educational
Publishing House.

12. 12
All information contained in this module are property of UCU and provided solely for educational purposes. Reproduction, storing in a retrieval system, distributing, uploading or posting online, or transmitting
in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise of any part of this document, without the prior written permission of UCU, is strictly prohibited.
NCM-116
Memory Tips
 Addison’s Disease
 Adrenal hypofunction usually due to autoimmune disease
 Initial Manifestation: Hypotension; bronze skin pigmentation is a common sign
 Laboratory Data: Hypoglycemia, hyponatremia, hyperkalemia
 Nursing Diagnosis: Fluid volume deficit
 Nursing Interventions:
 Monitor fluid and electrolyte balance
 Explain the need for lifelong medications of glucocorticoids and mineralocorticoids
 Maintain high sodium, low potassium diet
 Advise patient to avoid infection, trauma, or stress, it increases the risk for Addisonian crisis (IV hydrocortisone and saline
solution for Addisonian crisis)
 Cushing ‘s Syndrome
 Main Problem: Hypersecretion of the glucocorticoids by the adrenal glands
 Initial Manifestation: Central type or truncal obesity with thin extremities, moon face, buffalo hump, and hirsutism
 Laboratory data: Elevated serum cortisol levels, hyperglycemia, hypernatremia, hypokalemia, and hypertension
 Nursing Diagnosis: Altered skin integrity related to impaired healing
 Interventions:
 Maintain patient on high potassium and low sodium diet
 Instruct patient that treatment will involve lifelong administration of glucocorticoid synthesis inhibitors (Mitotane)
 Inform patient about slow wound healing
 Diabetes Insipidus
 Main Problem: Hyposecretion of antidiuretic hormone
 Initial manifestation: Polyuria, polydipsia
 Laboratory data: Fluid deprivation test confirms the disorder
 Nursing Diagnosis: Fluid Volume Deficit
 Interventions:
 Maintain Adequate fluid intake
 Monitor urine specific gravity
 Administer Desmopressin acetate intranasally as ordered
 Syndrome of Inappropriate antidiuretic Hormone (SIADH)
 Main Problem: Inappropriate continued release of antidiuretic hormone resulting in water intoxication
 Initial Manifestation: Mental Confusion
 Laboratory Data : Hyponatremia – Na , 120 mEq/L
 Nursing Diagnosis: Fluid Volume Excess
Fluid and electrolyte imbalance
 Interventions:
 Fluid Restriction
 Assess for signs and symptoms of hyponatremia
Review Questions