Nursing Management: Endocrine Problems Julie S. brinley, RN, MSN, CNE

Nursing Management:

Endocrine Problems

Julie S. brinley, RN, MSN, CNE

Disorders of the Anterior

• Acromegaly• Gigantism• Hypopituitarism• Dwarfism

Acromegaly

• Etiology and Pathophysiology– Overproduction of growth hormone (Usually

caused by benign pituitary tumor (adenoma)• Clinical Manifestations

– Depends on age

Acromegaly

Fig. 50-1. Progressive development of facial changes associated with acromegaly.

Acromegaly

• Diagnostic Studies– History and physical– Evaluation of plasma insulin (OGGT)– MRI and CT

• Collaborative Care– Surgical therapy

Acromegaly

Fig. 50-2. Surgery on the pituitary gland is most commonly performed with the transsphenoidal approach. Anincision is made in the inner aspect of the upper lip and gingiva. The sella turcica is entered through the floorof the nose and sphenoid sinuses.

Question

• Following a hypophysectomy for acromegaly, postoperative nursing care should focus on– A. Frequent monitoring of serum and urine

osmolarity.– B. Parenteral administration of a GH-receptor

antagonist.– C. Keeping the patient in a recumbent position at

all times.

Acromegaly

• Collaborative Care, continued– Radiation therapy– Drug therapy

• Sandostatin

Nursing Management: Acromegaly

• Nursing Assessment– s/s of abnormal issue growth and evaluate

changes in size of patient– Like What?

• Nursing Implementation– Post operative hypophysectomy– Life long hormone replacement therapy– Assess for DI because of possible damage to

posterior lobe

Hypofunction of Pituitary Gland

• Etiology and Pathophysiology– Tumor– Autoimmune disorder– Infection– Pituitary infarction (Sheehan syndrome)– Destruction of the pituitary gland – Can cause end-organ failure

• Clinical Manifestations and Diagnostic Studies– MRI, CT– Laboratory tests for specific hormone levels

Nursing and Collaborative Management: Hypofunction of Pituitary Gland

• Tumor removal with lifelong hormone replacement therapy

Disorders of Posterior Pituitary Gland

• SIADH (syndrome of inappropriate diuretic hormone)– Over production of ADH

• DI (Diabetes Insipidus)– Underproduction of ADH

Syndrome of Inappropriate Antidiuretic Hormone

• Etiology and Pathophysiology– Abnormal production of ADH

• Tumor CNS disorder• Drug therapy• Central nervous system disorders• Miscellaneous conditions• See table 50-1 page 1259


Fig. 50-3. Pathophysiology of syndrome of inappropriate antidiuretic hormone (SIADH).


• Clinical Manifestations and Diagnostic Studies– Fluid overload– Hyponatremia– Low urine output– Cerebral edema– Seizures and comaDiagnostic Studies– Serum sodium < 134– Serum osmolality < 280– Urine specific gravity > 1.005

Nursing and Collaborative Management: Syndrome of Inappropriate Antidiuretic Hormone

• Treat underlying cause• Fluid restriction• Hypertonic saline (slow infusion rate• Lop diuretics with supplements of K+, Ca+,

Mg++• Declomycin (blocks ADH• Vasopressin receptor antagonists

Question

• A patient with a head injury develops SIADH. Symptoms the nurse would expect to find include– A. Hypernatremia and edema.– B. Weight gain and decreased glomerular

filtration rate.– C. Muscle spasticity and hypertension.– D. Low urinary output and thirst

Diabetes Insipidus

• Etiology and Pathophysiology– Deficiency of ADH– Results in fluid and electrolyte loss– Neurogenic– Nephrogenic (lithium most common cause)– Psychogenic (excessive water intake)

Diabetes Insipidus

Fig. 50-4. Pathophysiology of diabetes insipidus (DI).

Diabetes Insipidus

• Clinical Manifestations– Polydipsia – Polyuria 5-20L/day– Low specific gravity– Serum osmolality > 295– Hypernatremia

• Diagnostic Studies– History and physical water restriction test

• How is this done? See page 1261

Nursing and Collaborative Management: Diabetes Insipidus

• Determine the cause• Replace fluids and electrolytes• Hormone replacement for central DI

– Vasopressin (DDAVP)• Nephrogenic

– Dietary measures (low-sodium diet)– Thiazide diuretics

Disorders of Thyroid Gland

Fig. 50-5. Continuum of thyroid dysfunction.

Hyperthyroidism

• A sustained increase in synthesis and release of thyroid hormones by thyroid gland

• Occurs more often in women• Highest frequency in 20- to 40-year-olds

Hyperthyroidism

• Most common form – Graves’ disease

• Other causes– Thyroiditis– Toxic nodular goiter– Exogenous iodine excess– Pituitary tumors– Thyroid cancer

Hyperthyroidism

• Thyrotoxicosis– Physiologic effects/clinical syndrome of

hypermetabolism resulting from increased circulating levels of T3, T4

• Hyperthyroidism and thyrotoxicosis occur together as Graves’ disease.

Etiology and Pathophysiology

Graves’ disease• Autoimmune disease of unknown origin

– Diffuse thyroid enlargement – Excessive thyroid hormone secretion


Graves’ disease (cont’d)• Precipitating factors

– Insufficient iodine supply– Infection– Stressful life events interacting with genetic

factors• Accounts for 75% of cases of hyperthyroidism


Graves’ disease (cont’d)• Antibodies are developed to TSH receptor.

– Leads to clinical manifestations of thyrotoxicosis – May progress to destruction of thyroid tissue,

causing hypothyroidism


Toxic nodular goiters• Thyroid hormone–secreting nodules independent of

TSH– If associated with hyperthyroidism, termed toxic

• Multiple or single nodules• Usually benign follicular adenomas• Occur equally in men and women

Clinical Manifestations

• Related to effect of thyroid hormone excess– ↑ metabolism– ↑ tissue sensitivity to stimulation by sympathetic

nervous system


• Ophthalmopathy– Abnormal eye appearance or function– Exophthalmos

• Protrusion of eyeballs from the orbits– Impaired drainage from orbit– Increased fat and edema in retroorbital tissues– Seen in 20% to 40% of patients

Exophthalmos and Goiter of Graves’ Disease

Fig. 50-6. Exophthalmos and goiter of Graves’ disease.


• Cardiovascular system– Bruit over thyroid gland– Systolic hypertension– ↑ cardiac output– Dysrhythmias– Cardiac hypertrophy– Atrial fibrillation


• GI system– ↑ appetite, thirst– Weight loss– Diarrhea– Splenomegaly – Hepatomegaly


• Integumentary system– Warm, smooth, moist skin– Thin, brittle nails– Hair loss– Clubbing of fingers– Diaphoresis– Vitiligo

Acropachy

Fig. 50-9. Thyroid acropachy. Digital clubbing and swelling of fingers.


• Musculoskeletal system– Fatigue– Muscle weakness– Proximal muscle wasting– Dependent edema– Osteoporosis


• Nervous system– Fine tremors– Insomnia – Ability of mood, delirium– Hyperreflexia of tendon reflexes– Inability to concentrate


• Reproductive system– Menstrual irregularities – Amenorrhea– Decreased libido– Impotence– Gynecomastia in men– Decreased fertility


• Intolerance to heat• ↑ sensitivity to stimulant drugs• Elevated basal temperature

Complications

Thyrotoxic crisis• Acute, rare condition, where all

manifestations are heightened• Life-threatening emergency• Death rare when treatment initiated • Presumed causes are additional stressors.

Complications

Thyrotoxic crisis• Manifestations include

– Tachycardia– Heart failure– Shock– Hyperthermia– Restlessness

Complications

Thyrotoxic crisis• Manifestations (cont’d)

– Agitation– Seizures– Abdominal pain– Nausea

Complications

Thyrotoxic crisis• Manifestations (cont’d)

– Vomiting – Diarrhea– Delirium– Coma

Complications

Thyrotoxic crisis• Treatment

– ↓ Thyroid hormone levels and clinical manifestations with drug therapy

• Therapy– Aimed at managing respiratory distress, fever

reduction, fluid replacement, and management of stressors

Diagnostic Studies

• History• Physical examination• Ophthalmologic examination• ECG• Radioactive iodine uptake (RAIU)

– Indicated to differentiate Graves’ disease from other forms of thyroiditis

Diagnostic Studies

• Laboratory tests– TSH– Free thyroxine (free T4)– Total T3 and T4

Collaborative Care

• Goals– Block adverse effects of thyroid hormones. – Stop hormone oversecretion.

Collaborative Care

• Three primary treatment options– Antithyroid medications– Radioactive iodine therapy (RAI)– Subtotal thyroidectomy

Collaborative Care

• Drug therapy– Useful in treatment of thyrotoxic states– Not considered curative

• Antithyroid drugs• Iodine• β-adrenergic blockers

Collaborative Care

• Antithyroid drugs– Inhibit synthesis of thyroid hormone – Improvement in 1 to 2 weeks – Good results in 4 to 8 weeks– Therapy for 6 to 15 months

Collaborative Care

• Antithyroid drugs (cont’d)– Disadvantages include

• Patient noncompliance• Increased rate of recurrence

– First-line examples• Propylthiouracil (PTU)

– Also blocks conversion of T4 to T3

• Methimazole (Tapazole)

Collaborative Care

• Iodine – Used with other antithyroid drugs in preparation

for thyroidectomy or treatment of crisis– Large doses rapidly inhibit synthesis of T3 and T4

and block their release into circulation.

Collaborative Care

• Iodine (cont’d) – ↓ vascularity of thyroid gland– Maximal effect seen within 1 to 2 weeks– Long-term iodine therapy is not effective.– Examples

• Saturated solution of potassium iodine (SSKI)• Lugol’s solution

Collaborative Care

• β-adrenergic blockers– Symptomatic relief of thyrotoxicosis resulting from

β-adrenergic receptor stimulation– Propranolol (Inderal) administered with other

antithyroid agents– Atenolol (Tenormin) is the preferred β-adrenergic

blocker for patients with asthma or heart disease.

Collaborative Care

• Radioactive iodine therapy (RAI)– Treatment of choice in nonpregnant adults

• Damages or destroys thyroid tissue

– Delayed response• 2 to 3 months

– Treated with antithyroid drugs and Inderal before and during first 3 months of RAI

Collaborative Care

• RAI (cont’d)– High incidence of posttreatment hypothyroidism– Need for lifelong thyroid hormone replacement

Collaborative Care

• Surgical therapy– Indications

• Unresponsive to drug therapy• Large goiters causing tracheal compression• Possible malignancy• Individual not a good candidate for RAI

Collaborative Care

• Surgical therapy (cont’d)– Subtotal thyroidectomy

• Preferred surgical procedure• Involves removal of significant portion of thyroid • 90% removed to be effective

Collaborative Care

• Surgical therapy (cont’d)– Endoscopic thyroidectomy appropriate with small

nodules and no malignancy– Less scarring, pain, and recovery time

Collaborative Care

• Surgical therapy (cont’d)– Before surgery

• Antithyroid drugs, iodine, and β-adrenergic blockers may be administered

– To achieve euthyroid state – To control symptoms

Collaborative Care

• Nutritional therapy– High-calorie diet may be ordered

• For hunger and prevention of tissue breakdown

– Protein allowance 1 to 2 g/kg ideal body weight– Avoid caffeine, highly seasoned foods, and high-

fiber foods

Nursing ManagementNursing Assessment

• Health history – Preexisting goiter – Recent infection or trauma– Immigration from iodine-deficient area– Medications– Family history of thyroid or autoimmune disorders


• Weight loss• Nausea• Diarrhea• Dyspnea on exertion• Muscle weakness• Insomnia• Heat intolerance


• Decreased libido• Impotence • Amenorrhea• Irritability• Personality changes• Delirium


• Objective Data– Agitation– Hyperthermia– Enlarged or nodular thyroid gland– Eyelid retraction– Diaphoretic skin


• Brittle nails• Edema• Tachypnea• Tachycardia• Hepatosplenomegaly


• Hyperreflexia• Fine tremors• Muscle wasting • Coma• Menstrual irregularities• Infertility

Nursing ManagementNursing Diagnoses

• Activity intolerance • Risk for injury• Imbalanced nutrition: Less than body

requirements• Anxiety• Insomnia

Nursing ManagementPlanning

• Overall goals– Experience relief of symptoms.– Have no serious complications related to disease

or treatment.– Maintain nutritional balance.– Cooperate with therapeutic plan.

Nursing ManagementNursing Implementation

• Acute intervention– Usually treated in outpatient setting– Those with acute thyrotoxicosis or undergoing

thyroidectomy require hospitalization and acute care.


• Acute thyrotoxicosis– Requires aggressive treatment– Administer medications to block thyroid hormone

production.– Administer IV fluids.– Ensure adequate oxygenation.


• Acute thyrotoxicosis (cont’d)– Calm, quiet room– Cool room– Light bed coverings


• Acute thyrotoxicosis (cont’d)– Change linens frequently if diaphoretic.– Encourage and assist with exercise.– Establish supportive relationship.– Apply artificial tears to relieve eye discomfort.– Elevate HOB and salt restriction for edema.


• Acute thyrotoxicosis (cont’d)– Do eye exercises.– Tape eyelids shut for sleep if they cannot close.– Wear dark glasses to reduce glare and prevent

environmental irritants.


• Thyroid surgery– Preoperative care

• Alleviate signs/symptoms of thyrotoxicosis.• Control cardiac problems.• Assess for signs of iodine toxicity.• Oxygen, suction equipment, and tracheostomy tray are

available in room.


• Thyroid surgery (cont’d)– Preoperative teaching

• Coughing, deep breathing, and leg exercises• Supporting head while turning in bed• Range-of-motion exercises of neck• Speaking difficulty for a short time after surgery• Routine postop care


• Thyroid surgery (cont’d)– Postoperative care

• Every 2 hours for 24 hours– Assess for signs of hemorrhage. – Assess for tracheal compression.

» Irregular breathing, neck swelling, frequent swallowing, choking

• Semi-Fowler’s position – Support head with pillows.– Avoid flexion of neck.– Tension on suture lines


• Thyroid surgery (cont’d)– Postoperative care

• Monitor vitals.• Control pain.• Check for tetany.

– Trousseau’s and Chvostek’s signs should be monitored.– Monitor for 72 hours.

• Evaluate difficulty in speaking/hoarseness.– Some hoarseness is expected for 3 to 4 days.


• Ambulatory and home care– Discharge teaching

• Monitor hormone balance periodically.• Decrease caloric intake to prevent weight gain.

– Adequate iodine

• Perform regular exercise.• Avoid ↑ environmental temperature.• Avoid goitrogens.


• Ambulatory and home care (cont’d)– Discharge teaching

• Regular follow-up care– Biweekly for a month and then semiannually

• After complete thyroidectomy– Lifelong thyroid replacement instruction

• Signs/symptoms thyroid failure

Nursing ManagementEvaluation

• Relief of symptoms• No serious complications related to disease or

treatment• Cooperate with therapeutic plan.

When assessing a patient who is returned to the surgical unit following a thyroidectomy, the nurse would be most concerned if the patient:

1. Complains of thirst. 2. States her throat is sore.3. Holds her head when she moves in bed. 4. Makes harsh, vibratory sounds when she breathes.

Question

Case Study

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Case Study

• 28-year-old woman visits her primary care physician’s office.

• She states she is always hungry, yet has lost 15 lbs in the past few months.

Case Study

• She also claims to always be tired.

• Her skin is warm and moist.

• Her nails have become brittle.

Case Study

• She has a bounding pulse and a slight heart murmur.

• Palpation of her thyroid reveals a nodular goiter.

Case Study

• Labs reveal– ↓ TSH– ↑ free thyroxine (free T4)

Discussion Questions

1. What problem do her symptoms and lab values suggest?

2. What treatments may the patient require?


3. What follow-up will she need with these treatments?

4. What important patient teaching should you do following these treatments?

Hypothyroidism

• One of the most common medical disorders in the United States

• Affects 1 in 50 women and 1 in 300 men


• Results from insufficient circulating thyroid hormone– Result of a variety of abnormalities


• Can be primary or secondary– Primary

• Related to destruction of thyroid tissue or defective hormone synthesis

– Secondary• Related to pituitary disease with ↓ TSH secretion or

hypothalamic dysfunction

94


• May be transient, related to thyroiditis, or result from discontinuing thyroid hormone therapy


• Iodine deficiency – Most common cause worldwide and is most

prevalent in iodine-deficient areas• In places where iodine intake is adequate, the

primary cause is atrophy of the gland.


• May also develop because of treatment for hyperthyroidism

• Amiodarone and lithium can produce hypothyroidism.


• Cretinism is caused by thyroid hormone deficiencies during fetal or neonatal life.

• All infants are screened at birth for ↓ thyroid function.


• Vary depending on – Severity– Duration– Age of onset

• Systemic effects characterized by slowing of body processes


• Ranges from no symptoms to classic symptoms and physical changes easily detected on examination


• Onset of symptoms may occur over months to years.– Unless occurs after thyroidectomy, thyroid

ablation, treatment with antithyroid drugs


• Cardiovascular system– ↓ cardiac output– ↓ cardiac contractility– Anemia– Cobalamin, iron, folate deficiencies– ↑ serum cholesterol and triglycerides


• Respiratory system– Low exercise tolerance– Shortness of breath on exertion


• Neurologic system– Fatigued and lethargic– Personality and mood changes– Impaired memory, slowed speech, decreased

initiative, and somnolence


• Gastrointestinal system– ↓ motility– Achlorhydria – Constipation


• Other changes– Cold intolerance– Hair loss– Dry/coarse skin– Brittle nails– Hoarseness– Muscle weakness and swelling– Weight gain– Menorrhagia


• Those with severe long-standing hypothyroidism may display myxedema.– Accumulation of hydrophilic mucopolysaccharides

in the dermis and other tissues– Causes puffiness, periorbital edema, masklike

effect

Common Features of Myxedema

Fig. 50-10. Common features of myxedema. Dull, puffy skin; coarse, sparse hair; periorbital edema; andprominent tongue.

Complications

• Mental sluggishness• Drowsiness• Lethargy progressing gradually or suddenly to

impairment of consciousness or coma– Myxedema coma

Diagnostic Studies

• History and physical examination• Laboratory tests

– Serum TSH• Determines cause of hypothyroidism

– Free T4– Serum T3 – Serum T4

Diagnostic Studies

• Laboratory findings (cont’d)– Other abnormal findings are

↑ cholesterol and triglycerides, anemia, and ↑ creatine kinase.

Diagnostic Studies

• TRH stimulation test– ↑ in TSH after TRH injection suggests

hypothalamic dysfunction.– No change after TRH injection suggests anterior

pituitary dysfunction.

Collaborative Care

• Restoration of euthyroid state as safely and rapidly as possible

• Low-calorie diet

Collaborative Care

• Levothyroxine (Synthroid)– Must take regularly– Monitor for angina and cardiac dysrhythmias.

• Monitor thyroid hormone levels, and adjust (as needed).

• Liotrix (Thyrolar)

Question

• The health care provider prescribes levothyroxine for a patient with hypothyroidism. Following teaching regarding this drug, the nurse determines that further instruction is needed when the patient says,– A. “I will report any chest pain or difficulty breathing to the

doctor right away.”– B. “I can expect to return to normal function with the use of

this drug.”– C. “I only need to take this drug until my symptoms are

improved.” – D. “I can expect the medication dose may need to be

increased.”


• Health history– Weight gain– Mental changes– Fatigue– Slowed/slurred speech – Cold intolerance– Skin changes


• Health history (cont’d)– Constipation– Dyspnea– Recent introduction of iodine medications


• Physical examination– Bradycardia– Distended abdomen– Dry, thick, cold skin– Thick, brittle nails– Paresthesias– Muscular aches and pains

Nursing ManagementNursing Diagnoses

• Imbalanced nutrition: More than body requirements

• Activity intolerance• Impaired memory

Nursing ManagementPlanning

• Experience relief of symptoms.• Maintain a euthyroid state.• Maintain a positive self-image.• Comply with lifelong thyroid replacement

therapy.


• Health promotion– No consensus for thyroid function screening– High-risk populations screened for subclinical

thyroid disease• Family history of thyroid disease, history of neck

radiation, women over 50, and postpartum


• Acute intervention– Most individuals do not require acute nursing

care. • Managed on outpatient basis


• Acute intervention (cont’d)– Individual with myxedema coma requires acute

nursing care.• Mechanical respiratory support• Cardiac monitoring• IV thyroid hormone replacement• If hyponatremic, hypertonic saline may be

administered.• Monitor core temperature.


• Acute intervention (cont’d)– Individual with myxedema coma (cont’d)

• Vital signs• Weight• I & O• Visible edema• Cardiovascular response to hormone• Energy level• Mental alertness


• Ambulatory and home care– Explain nature of thyroid hormone deficiency and

self-care practices to prevent complications.• Patient and family must understand replacement

therapy and that it is lifelong.


• Ambulatory and home care (cont’d)– Teach measures to prevent skin breakdown.– Emphasize need for warm environment.– Caution patient to avoid sedatives or use lowest

dose possible.


• Ambulatory and home care (cont’d)– Discuss measures to minimize constipation.

• Avoid enemas because of vagal stimulation in cardiac patient.


• Ambulatory and home care (cont’d)– Teach patient to notify physician immediately if

signs of overdose appear.• Orthopnea, dyspnea, rapid pulse, palpitations,

nervousness, insomnia


• Ambulatory and home care (cont’d)– Patient with diabetes should test capillary blood

glucose at least daily. • Return to euthyroid state frequently.

↑ insulin requirements.


• Ambulatory and home care (cont’d)– Thyroid preparations potentiate the effects of

some common drug groups. • Teach patient toxic signs and symptoms of these drugs.

– Anticoagulants– Digitalis compounds


• Ambulatory and home care (cont’d)– Provide handouts that include verbal instructions

for patients and family members.

Nursing ManagementEvaluation

• Expected outcomes– Have relief from symptoms.– Maintain euthyroid state as evidenced by normal

thyroid hormone and TSH levels.– Adhere to lifelong therapy.

Case Study

133

Case Study

• 38-year-old woman enters a community outpatient clinic.

• She is complaining of overwhelming fatigue that is not relieved by rest.

Case Study

• She is attending graduate school and is very sedentary.

• She is so exhausted that she has difficulty waking for classes and trouble concentrating when studying.

Case Study

• Her face is puffy, and her skin is dry and pale.

• She is dressed inappropriately for warm weather.

Case Study

• She also complains of generalized body aches and pains with frequent muscle cramps and constipation.

Case Study

• Vital signs– BP 142/84– Heart rate 52– Respiratory rate 12– Temperature 96.8° F


1. What are some possible causes of her symptoms?


2. No obvious irregularities are found in her cardiopulmonary assessment. Her TSH levels come back to 20.9 IU/L. She is diagnosed with hypothyroidism. What can you tell her about the treatment and follow-up?


3. What teaching will you need to do with her before she leaves the clinic?

Goiter

Table 50-4. Drugs that are Goitrogens.

Thyroid Nodules and Cancer

• Types of Thyroid Cancer• Clinical Manifestations and Diagnostic Studies

Thyroid Nodules and Cancer

Fig. 50-7. A large “cold” nodule on the thyroid gland (arrow) detected by a scan.

Thyroiditis

Fig. 50-8. Hashimoto’s thyroiditis.

Hyperthyroidism

• Etiology and Pathophysiology– Graves’ disease– Toxic nodular goiters

• Clinical Manifestations

Hyperthyroidism

• Complications• Diagnostic Studies

Hyperthyroidism

• Collaborative Care – Drug therapy

• Antithyroid drugs• Iodine• Β adrenergic blockers‑

– Radioactive iodine therapy– Surgical therapy– Nutritional therapy

Nursing Management: Hyperthyroidism

• Nursing Assessment • Nursing Diagnoses• Planning

Nursing Management: Hyperthyroidism

• Nursing Implementation– Acute intervention

• Acute thyrotoxicosis• Thyroid surgery

– Ambulatory and home care• Postoperative care

• Evaluation

Hypothyroidism

• Etiology and Pathophysiology• Clinical Manifestations

DISORDERS OF PARATHYROID GLANDS

Hyperparathyroidism

• Etiology and Pathophysiology– Primary or secondary

• Clinical Manifestations and Complications• Diagnostic Studies

– Serum calcium (high)and phosphorus levels (low)– Bone x-rays and bone density tests

• Collaborative Care– Surgical therapy– Nonsurgical therapy

Nursing Management:Hyperparathyroidism

• Parathyroidectomy– Similar to that of thyroidectomy

Hypoparathyroidism

• Usually due to removal of parathyroid gland– (iatrogenic)

Nursing and Collaborative Management:Hypoparathyroidism

• Give IV calcium chloride or calcium gluconate (slowly)

• Vit D

Disorders of Adrenal Cortex

Focus onCushing Syndrome and Addison’s

Disease

Disorders of the Adrenal CortexCorticosteroids

• Adrenal cortex steroid hormones– Glucocorticoids

• Regulate metabolism and ↑ blood glucose• Critical to physiologic stress response

– Mineralocorticoids regulate • Sodium balance• Potassium balance

Disorders of the Adrenal CortexCorticosteroids

• Adrenal cortex steroid hormones– Androgen contributes to

• Growth and development in both genders • Sexual activity in adult women

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Cushing SyndromeEtiology and Pathophysiology

• Caused by excess of corticosteroids, particularly glucocorticoids

• Most common cause– Iatrogenic administration of exogenous

corticosteroids

Cushing Syndrome

Table 50-13. Causes of Cushing Syndrome.


• 85% of endogenous cases due to ACTH-secreting pituitary tumor

• Other causes include – Adrenal tumors – Ectopic ACTH production in tumors outside

hypothalamic-pituitary- adrenal axis • Usually lung and pancreas tumors


• Cushing disease and primary adrenal tumors are more common in women aged 20 to 40.

• Ectopic ACTH production is more common in men.

Cushing SyndromeClinical Manifestations

• Related to excess corticosteroids• Weight gain most common feature

– Trunk (centripetal obesity)– Face (“moon face”)– Cervical area– Transient weight gain from sodium and water

retention


Fig. 50-11. Cushing syndrome. Facies include a rounded face (“moon face”) with thin, reddened skin. Hirsutismmay also be present.


Fig. 50-12. Common characteristics of Cushing syndrome.


• Hyperglycemia – Glucose intolerance associated with cortisol-

induced insulin resistance– Increased gluconeogenesis by liver


• Protein wasting– Catabolic effects of cortisol– Leads to weakness, especially in extremities– Protein loss in bones leads to osteoporosis, bone

and back pain.

Question

• Which client history is most significant in the development of symptoms for a client who has iatrogenic Cushing’s disease:– A. Long-term use of anabolic steroids.– B. Extended use of inhaled steroids for asthma.– C. History of long-term glucocorticoid use.– D. Family history if increased cortisol production.


• Loss of collagen• Wound healing delayed• Mood disturbances• Insomnia• Irrationality• Psychosis


• Mineralocorticoid excess may cause hypertension secondary to fluid retention.

• Adrenal androgen excess may cause– Pronounced acne– Virilization in women– Feminization in men


• Seen more commonly in adrenal carcinomas– Women: Menstrual disorders and hirsutism– Men: Gynecomastia and impotence

• Purplish red striae on abdomen, breast, or buttocks


Fig. 50-13. Cushing syndrome. Truncal obesity; broad, purple striae; and easy bruising (left antecubital fossa).

Cushing SyndromeDiagnostic Studies

• 24-Hour urine for free cortisol– Levels above 80 to 120 mcg/day in adults indicate

Cushing syndrome.• Low-dose dexamethasone suppression test

used for borderline results of 24-hour urine cortisol


• False-positives can occur with depression and with certain drugs.

• Plasma cortisol levels may be elevated with loss of diurnal variation.

• CT and MRI of pituitary and adrenal glands


• Hypokalemia and alkalosis are seen in ectopic ACTH syndrome and adrenal carcinoma.

• Plasma ACTH may be low, normal, or elevated, depending on problem.


• Associated findings that are not diagnostic of Cushing syndrome– Leukocytosis– Lymphopenia– Eosinopenia– Hyperglycemia


• Associated findings that are not diagnostic of Cushing (cont’d)– Glycosuria– Hypercalciuria– Osteoporosis

Cushing SyndromeCollaborative Care

• Primary goal is to normalize hormone secretion.

• Treatment depends on cause.– Pituitary adenoma

• Surgical removal of tumor and/or radiation– Adrenal tumors or hyperplasia

• Adrenalectomy


• Treatment (cont’d)– Ectopic ACTH-secreting tumors

• Managed by treating primary neoplasm

• Drug therapy indicated when surgery is contraindicated or as adjunct to surgery

• Goal of drug therapy is inhibition of adrenal function.


• If Cushing syndrome develops during use of corticosteroids– Gradually discontinue therapy– Decrease dose– Convert to an alternate-day regimen

• Gradual tapering avoids potentially life-threatening adrenal insufficiency.

Cushing SyndromeNursing Assessment

• Patient medical history – Pituitary tumor– Adrenal, pancreatic, or pulmonary neoplasms– GI bleeding– Frequent infections


• Use of corticosteroids• Weight gain• Anorexia• Polyuria• Prolonged wound healing• Weakness, fatigue


• Easy bruising • Insomnia• Headache, back, joint, bone, and rib pain• Amenorrhea• Impotence


• Mood disturbances, anxiety, psychosis, poor concentration

• Truncal obesity• Buffalo hump• Moon face• Hirsutism of body and face


• Thinning of head hair• Thin, friable skin• Acne• Petechiae• Purpura• Hyperpigmentation


• Purplish red striae on breasts, buttocks, and abdomen

• Edema of lower extremities• Hypertension• Muscle wasting• Thin extremities• Awkward gait

Cushing SyndromeNursing Diagnoses

• Risk for infection• Imbalanced nutrition• Disturbed body image• Impaired skin integrity

Cushing SyndromeNursing Planning

• Patient goals include – Experience relief of symptoms– Have no serious complications– Maintain positive self-image– Actively participate in therapeutic plan

Cushing SyndromeNursing Implementation

• Health promotion– Identify patients at risk for Cushing syndrome.– Long-term exogenous cortisol therapy is major risk

factor.– Teach patients about medication use and to

monitor for side effects.


• Acute intervention– Assessment of

• Signs and symptoms of hormone and drug toxicity

• Complicating conditions– Cardiovascular disease– Diabetes mellitus– Infection


• Acute intervention (cont’d)– Monitor

• Vital signs • Daily weight• Glucose• Infection• Signs and symptoms of abnormal thromboembolic

phenomena


• Emotional support– Patient may feel unattractive or unwanted.– Nursing staff should remain sensitive to patient’s

feeling and be respectful.– Reassure patient that physical symptoms will

resolve when hormone levels return to normal.


• Preoperative care– Patient should be in optimal physical condition.– Control hypertension and hyperglycemia. – Hypokalemia must be corrected with diet and

potassium supplements.


• Preoperative care (cont’d)– High-protein diet helps correct protein depletion. – Teaching depends on surgical approach.


• Preoperative care (cont’d)– Include information on postoperative care.

• Nasogastric tube• Urinary catheter• IV therapy• Central venous pressure monitoring• Leg compression devices


• Postoperative care– Risk of hemorrhage is increased because of high

vascularity of adrenal glands.– Manipulation of glandular tissue may release

hormones into circulation.– BP, fluid balance, and electrolyte levels tend to be

unstable because of hormone fluctuations.


• Postoperative care (cont’d)– High doses of corticosteroids administered by IV

during and several days after surgery – Report any significant changes in

• BP• Respiration• Heart rate


• Postoperative care (cont’d)– Monitor fluid intake and output to assess for

imbalances.– Critical period for circulatory instability ranges

from 24 to 48 hours.– Morning urine levels of cortisol are measured to

evaluate the effectiveness of surgery.


• Postoperative care (cont’d)– Adrenal insufficiency develops if corticosteroid

dosage is tapered rapidly.– Indications of hypocortisolism

• Vomiting• Increased weakness• Dehydration• Hypotension


• Postoperative care (cont’d)– Patient may complain of

• Painful joints• Pruritus• Peeling skin• Severe emotional disturbances


• Postoperative care (cont’d)– Bed rest until BP is stabilized after surgery– Meticulous care should be taken when accessing

skin, circulation, or body cavities to avoid infection.

• Normal inflammatory responses are suppressed.


• Ambulatory and home care– Discharge instructions based on lack of

endogenous corticosteroids– Wear Medic Alert bracelet at all times.– Avoid exposure to stress, extremes of

temperature, and infection.– Lifetime replacement therapy is required for many

patients.

Cushing SyndromeNursing Evaluation

• Expected outcomes– Experience no signs or symptoms of infection.– Attain weight appropriate for height.– Increase acceptance of appearance.– Maintain intact skin.

An IV hydrocortisone infusion is started before a patient is taken to surgery for a bilateral adrenalectomy. The nurse explains to the patient that this is done to:

1. Prevent sodium and water retention after surgery.2. Prevent clots from forming in the legs during recovery from

surgery.3. Provide substances to respond to stress after removal of the

adrenal glands.4. Stimulate the inflammatory response to promote wound

healing.

Question

Case Study

207

Case Study

• You are working with a home care agency and visiting a 60-year-old man with COPD related to cigarette smoking.

Case Study

• He has been on home oxygen for several years.

• He began oral steroid therapy 10 months ago.

Case Study

• In addition to his usual signs and symptoms due to COPD, you observe some new findings during your assessment.

• His BP is 180/94.

Case Study

• He has striae over his trunk and thighs.

• He has a full-looking face.

• He has developed truncal obesity with supraclavicular and posterior upper back fat and thin extremities.

Case Study Discussion Questions

1. What syndrome has he likely developed?

2. What is the most probable cause of this change?

3. What is his primary nursing management?


4. Cushing syndrome can affect memory. Patients can easily forget to take medications. What can you do to help him remember to take his pills as prescribed?

Focus on Addison’s Disease

Addison’s DiseaseEtiology and Pathophysiology

• Adrenocortical insufficiency may – Be Addison’s disease

• Primary

– Result from lack of pituitary ACTH• Secondary


• All three classes of adrenal corticosteroids are ↓ in Addison’s disease. – Glucocorticoids– Mineralocorticoids– Androgens


• Common cause is autoimmune response to adrenal tissue.

• Susceptibility genes beginning to be identified• Other endocrine conditions often found


• Other causes of Addison’s disease– Tuberculosis (rare in North America)– Infarction– Fungal infection– AIDS– Metastatic cancer


• Iatrogenic Addison’s disease may be due to adrenal hemorrhage.– Anticoagulant therapy– Antineoplastic chemotherapy– Nizoral therapy for AIDS– Bilateral adrenalectomy


• Most often occurs in adults <60 years old • Affects both genders equally• More common in white females if from

autoimmune response

Addison’s DiseaseClinical Manifestations

• Does not become evident until 90% of adrenal cortex is destroyed

• Disease usually advanced before diagnosis


• Primary features – Progressive weakness– Fatigue– Weight loss– Anorexia – Skin hyperpigmentation

Hyperpigmentation

Fig. 50-14. Hyperpigmentation typically seen in Addison’s disease.


• Orthostatic hypotension • Hyponatremia • Hyperkalemia• Nausea and vomiting• Diarrhea• Irritability, depression


• Secondary adrenocortical hypofunction– Signs and symptoms common with Addison’s

disease– Patients characteristically lack hyperpigmentation.

Addison’s DiseaseComplications

• Risk for life-threatening addisonian crisis caused by – Insufficient adrenocortical hormones – Sudden, sharp decrease in these hormones

• Triggered by– Stress– Withdrawal of hormone replacement– After adrenal surgery– Following sudden pituitary gland destruction


• Severe manifestations of glucocorticosteroid and mineralocorticoid deficiencies– Hypotension– Tachycardia– Dehydration– Hyponatremia


• Manifestations (cont’d)– Hyperkalemia– Hypoglycemia– Fever– Weakness– Confusion


• Hypotension can lead to shock. • Circulatory collapse is often unresponsive to

usual treatment. • GI manifestations include severe vomiting,

diarrhea, and abdominal pain.• Pain in lower back or legs

Addison’s DiseaseDiagnostic Studies

• Subnormal levels of cortisol • Levels fail to rise over basal levels with ACTH

stimulation test.– Latter indicates primary adrenal disease. – Positive response to ACTH stimulation indicates

functioning adrenal gland.


• Abnormal laboratory findings– Hyperkalemia– Hypochloremia– Hyponatremia– Hypoglycemia


• Abnormal laboratory findings (cont’d)– Anemia– ↑ BUN– Low urine cortisol levels


• Other abnormal findings – ECG

• Low voltage, vertical QRS axis, peaked T waves from hyperkalemia

• CT and MRI used to– Localize tumors – Identify adrenal calcifications or enlargement

Addison’s DiseaseCollaborative Care

• Hydrocortisone – Most commonly used as replacement therapy

• Glucocorticoid dosage must be ↑ during times of stress to prevent addisonian crisis.

Addison’s DiseaseCollaborative Care

• Addisonian crisis – Treatment directed at

• Shock management• High-dose hydrocortisone replacement

Addison’s DiseaseNursing Implementation

• Acute intervention– Frequent assessment necessary– Assess vital signs and signs of fluid and electrolyte

imbalance every 30 minutes to 4 hours for first 24 hours.

– Take daily weights.– Administer corticosteroid therapy diligently.


• Acute intervention (cont’d)– Protect against infection.– Assist with daily hygiene.– Protect from extremes.

• Light• Noise• Temperature


• Ambulatory and home care– Glucocorticoids usually given in divided doses – Mineralocorticoids given once in the morning

• Reflects normal circadian rhythm• Decreases side effects of corticosteroids


• Ambulatory and home care (cont’d)– Long-term care includes need for

• Extra medication• Stress management


• Ambulatory and home care (cont’d)– Situations requiring corticosteroid dose

adjustment include • Fever• Influenza• Tooth extraction• Physical exertion


• Ambulatory and home care (cont’d)– Doses are doubled for minor stressors and tripled

for major stressors.– It is better to err on the side of overreplacement.


• Instruct on how to take BP and report findings.• Carry emergency kit with IM hydrocortisone,

syringes, and instructions for use.– Teach patient and significant others how to give

IM injection.

Corticosteroid TherapyEffects of Corticosteroid Therapy

• Long-term use of corticosteroids can lead to complications and side effects.

• Reserved for cases with risk of death or loss of function

• Potential benefits must be weighed against risks.

Corticosteroid TherapyEffects of Corticosteroid Therapy

• Expected effects of corticosteroid therapy– Antiinflammatory action– Immunosuppression– Maintenance of normal BP– Carbohydrate and protein metabolism

Corticosteroid TherapyManagement

• Should be taken in the morning with food to reduce gastric irritation

• Must not be stopped abruptly• Assess for corticosteroid-induced

osteoporosis.

Hyperaldosteronism Etiology and Pathophysiology

• Excessive aldosterone secretion– Sodium retention– Potassium– Hydrogen ion excretion

• Hallmark of hyperaldosteronism– Hypertension with hypokalemic alkalosis

Hyperaldosteronism Etiology and Pathophysiology

• Primary hyperaldosteronism – Usually caused by solitary adrenocortical adenoma

• Secondary hyperaldosteronism – Due to renal artery stenosis,

renin-secreting tumors, and chronic kidney disease

Hyperaldosteronism Clinical Manifestations

• Elevated levels of aldosterone – Sodium retention– Elimination of potassium

• Sodium retention leads to– Hypernatremia– Hypertension– Headache


• Eliminating potassium leads to– Hypokalemia– Muscle weakness– Fatigue– Cardiac dysrhythmias


• Eliminating potassium (cont’d)– Glucose intolerance– Metabolic alkalosis– May lead to tetany

Hyperaldosteronism Diagnostic Studies

• Primary aldosteronism– ↑ plasma aldosterone levels– ↑ sodium levels– ↓ potassium levels– ↓ renin activity

• Adenomas are localized by CT or MRI.

Hyperaldosteronism Treatment

• Preferred treatment for primary hyperaldosteronism is surgical removal of the adenoma.

Hyperaldosteronism Treatment

• Before surgery, patients need – Low-sodium diet– Potassium-sparing diuretics– Antihypertensive agents

• Assess – BP– Fluid/electrolyte balance

Pheochromocytoma Etiology and Pathophysiology

• Caused by a tumor of the adrenal medulla• Produces excessive catecholamines• Most often in young to middle-aged adults

S/S Pheochrocytoma

• Headaches (severe) • Excess sweating (generalized) • Racing heart (tachycardia and palpitations) • Anxiety / nervousness (feelings of impending death) • Nervous shaking (tremors) • Pain in the lower chest or upper abdomen • Vomiting (with or without nausea) • Weight loss • Heat intolerance

Diagnosis Pheochromoctyoma

• 24 hour urinary catacholamines and metanephrines. This study is designed to measure production of the different types of adrenaline compounds that the adrenal makes. Since the body gets rid of these hormones in the urine, we simply collect a patient's urine for 24 hours and determine if they are over-produced. This test measures different types of adrenaline (epinephrine, norepinephrine, dopamine) as well as the break-down products of these compounds which the liver and kidney have degraded. Since these compounds are concentrated in the urine, this test is very good at making the diagnosis of pheochromocytomas.

Pheochromocytoma Clinical Manifestations

• Clinical features include– Severe, episodic hypertension– Severe, pounding headache– Tachycardia with palpitations– Profuse sweating– Abdominal or chest pain

• Diagnosis is often missed.

Pheochromocytoma Diagnostic Studies

• Best test is measurement of urinary fractionated metanephrines and catecholamines in 24-hour collection.

• Serum catecholamines are elevated.• CT and MRI are used for tumor localization.

Pheochromocytoma Treatment

• Surgical removal of tumor• Calcium channel blockers control BP.• Sympathetic blocking agents may

– ↓ BP – ↓ symptoms of catecholamine excess

• Beta blockers to ↓ dysrhythmias


• Monitor BP closely.• Make patient as comfortable as possible.• Monitor glucose.


• Patient needs – Rest– Nourishment– Emotional support

• Stress importance of – Follow-up care – Routine BP monitoring

The nurse determines that the patient in acute adrenal insufficiency is responding favorably to treatment when:

1. The patient appears alert and oriented.2. The patient’s urinary output has increased.3. Pulmonary edema is reduced as evidenced by clear lung

sounds.4. Laboratory tests reveal elevations of potassium and

glucose serum levels and a decrease in the sodium level.

Question

Case Study

263

Case Study

• 30-year-old woman arrives to the ED with syncope after standing up.

• Her skin is hyperpigmented over her joints and on her palms.

Case Study

• Lab values reveal– ↓ ACTH– ↓ plasma cortisol– ↓ Na– ↓ glucose– ↑ K


1. Based on the findings, what are her possible diagnoses?

2. What is her primary acute nursing management?


3. What critical patient teaching should you do with her about her home care?

4. What lifestyle modifications should she make?

Documents

Nursing Management: Endocrine Problems Julie S. brinley, RN, MSN, CNE