Nursing Management: Endocrine Problems

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

Disorders of the Anterior
Acromegaly Gigantism Hypopituitarism Dwarfism

Acromegaly Etiology and Pathophysiology Clinical Manifestations
Overproduction of growth hormone (Usually caused by benign pituitary tumor (adenoma) Clinical Manifestations Depends on age

Acromegaly Fig Progressive development of facial changes associated with acromegaly.

Acromegaly Diagnostic Studies Collaborative Care History and physical
Evaluation of plasma insulin (OGGT) MRI and CT Collaborative Care Surgical therapy

Acromegaly Fig Surgery on the pituitary gland is most commonly performed with the transsphenoidal approach. An incision is made in the inner aspect of the upper lip and gingiva. The sella turcica is entered through the floor of 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. A need to monitor for DI from damage to the posterior pituitary gland (lack of ADH)

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 Pathophysiology of syndrome of inappropriate antidiuretic hormone (SIADH).

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

Treat underlying cause Fluid restriction
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 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 Pathophysiology of diabetes insipidus (DI).

Diabetes Insipidus Clinical Manifestations Diagnostic Studies
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 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 Other causes Graves’ disease
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 These antibodies attach to the receptors and stimulate the thyroid gland to release T3, T4, or both. The disease is characterized by remissions and exacerbations with or without treatment.

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 Although they can appear at any age, the frequency of toxic multinodular goiter is greatest in people over 40 years of age.

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 {See next slide for figure.} Exophthalmos is a type of infiltrative ophthalmopathy that is due to impaired venous drainage from the orbit, which causes increased fat deposits and fluid (edema) in the retroorbital tissues. Increased pressure forces the eyeballs outward.

Exophthalmos and Goiter of Graves’ Disease
In ophthalmopathy, the upper lids are usually retracted and elevated, with the sclera visible above the iris. When the eyelids do not close completely, the exposed corneal surfaces become dry and irritated. Fig Exophthalmos and goiter of Graves’ disease.

Cardiovascular system Bruit over thyroid gland Systolic hypertension ↑ cardiac output Dysrhythmias Cardiac hypertrophy Atrial fibrillation Manifestations of thyroid hyperfunction are summarized in Table 50-5.

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 Digital clubbing and swelling of fingers Fig 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 Therapy
↓ 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 The two primary laboratory findings used to confirm the diagnosis of hyperthyroidism are decreased TSH levels and elevated free thyroxine (free T4) levels.

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 In general, the treatment of choice is radioactive iodine therapy. However, the choice of treatment is influenced by the patient’s age and preferences, severity of the disorder, and complicating features (including pregnancy).

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) PTU lowers hormone levels more quickly but must be taken 3 times per day. Tapazole is administered in a single daily dose. Indications for the use of antithyroid drugs include Graves’ disease in the young patient, hyperthyroidism during pregnancy, and the need to achieve a euthyroid state before surgery or radiation therapy.

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 RAI therapy is administered on an outpatient basis. Because the therapeutic dose of radioactive iodine is low, no radiation safety precautions are necessary.

Collaborative Care Surgical therapy Indications
Unresponsive to drug therapy Large goiters causing tracheal compression Possible malignancy Individual not a good candidate for RAI One advantage thyroidectomy has over RAI is a more rapid reduction in T3 and T4 levels.

Collaborative Care Surgical therapy (cont’d) Subtotal thyroidectomy
Preferred surgical procedure Involves removal of significant portion of thyroid 90% removed to be effective If too much tissue is taken, the gland will not regenerate after surgery and hypothyroidism will result.

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 Postoperative complications include hypothyroidism, damage to or inadvertent removal of parathyroid glands causing hypoparathyroidism and hypocalcemia, hemorrhage, injury to the recurrent or superior laryngeal nerve, thyrotoxic crisis, and infection.

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 A high-calorie diet may involve 4000 to 5000 cal/day. This can be accomplished with six full meals a day and snacks high in protein, carbohydrates, minerals, and vitamins, particularly vitamin A, thiamine, vitamin B6, and vitamin C. Increase carbohydrate intake to compensate for increased metabolism.

Nursing Management Nursing Assessment
Health history Preexisting goiter Recent infection or trauma Immigration from iodine-deficient area Medications Family history of thyroid or autoimmune disorders Subjective and objective data that should be obtained from an individual with hyperthyroidism are presented in Table 50-9.

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 Management Nursing Diagnoses
Activity intolerance Risk for injury Imbalanced nutrition: Less than body requirements Anxiety Insomnia

Nursing Management Planning
Overall goals Experience relief of symptoms. Have no serious complications related to disease or treatment. Maintain nutritional balance. Cooperate with therapeutic plan.

Nursing Management Nursing 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. Monitor for cardiac dysrhythmias and decompensation, ensure adequate oxygenation, and administer IV fluids to replace fluid and electrolyte losses.

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. Elevate the patient’s head to promote fluid drainage from the periorbital area; the patient should sit upright as much as possible. If exophthalmos is severe, corticosteroids, radiation of retroorbital tissues, orbital decompression, or corrective lid or muscle surgery may be used.

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. If toxicity occurs, iodine administration should be discontinued and the health care provider notified.

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. Most patients experience a period of relative hypothyroidism soon after surgery because of the substantial reduction in the size of the thyroid. However, the remaining tissue usually hypertrophies, recovering the capacity to produce hormones, but this takes time. Seafood once or twice a week or normal use of iodized salt should provide sufficient iodine intake.

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 Management Evaluation
Relief of symptoms No serious complications related to disease or treatment Cooperate with therapeutic plan.

Question 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. Answer: 4 Rationale: After thyroid surgery, the patient may experience an airway obstruction related to excess swelling, hemorrhage, hematoma formation, or laryngeal stridor (harsh, vibratory sound). The patient should have emergency equipment at the bedside, including oxygen, suction equipment, and a tracheostomy tray.

Case Study 84

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 What problem do her symptoms and lab values suggest? What treatments may the patient require? Hyperthyroidism. RAI, antithyroid drugs, or iodine.

Discussion Questions What follow-up will she need with these treatments? What important patient teaching should you do following these treatments? 3. She will need to monitor her thyroid hormone levels regularly to avoid hypothyroidism. 4. The importance of follow-up care and monitoring of thyroid hormone levels.

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

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. This atrophy is the end result of Hashimoto’s thyroiditis and Graves’ disease.

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 The severity of symptoms depends on the degree of thyroid hormone deficiency and the long-term physiologic effects of thyroid hormone deficiency. The patient is often fatigued and lethargic, and experiences personality and mental changes. Many individuals with hypothyroidism appear depressed. Although the patient with hypothyroidism sleeps for long periods of time, the stages of sleep are altered.

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 Constipation, which is a common complaint, may progress to obstipation and, rarely, to intestinal obstruction.

Other changes Cold intolerance Hair loss Dry/coarse skin Brittle nails Hoarseness Muscle weakness and swelling Weight gain Menorrhagia Weight gain is most likely a result of decreased metabolic rate.

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 {See next slide for figure.} Individuals with hypothyroidism may describe an impaired self-image related to their disabilities and altered appearance.

Common Features of Myxedema
Dull, puffy skin; coarse, sparse hair; periorbital edema; and prominent tongue Fig Common features of myxedema. Dull, puffy skin; coarse, sparse hair; periorbital edema; and prominent tongue.

Complications Mental sluggishness Drowsiness
Lethargy progressing gradually or suddenly to impairment of consciousness or coma Myxedema coma Myxedema coma can be precipitated by infection, drugs (especially opioids, tranquilizers, and barbiturates), exposure to cold, and trauma. It is characterized by subnormal temperature, hypotension, and hypoventilation. For the patient to survive, vital functions must be supported and IV thyroid hormone replacement must be administered.

Diagnostic Studies History and physical examination Laboratory tests
Serum TSH Determines cause of hypothyroidism Free T4 Serum T3 Serum T4 The presence of thyroid peroxidase antibodies suggests an autoimmune origin of the problem.

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) Any chest pain experienced by a patient starting thyroid replacement should be reported immediately, and an electrocardiogram (ECG) and serum cardiac enzyme tests must be performed. In the patient without side effects, the dose is increased at 4- to 6-week intervals. It is important that the patient take replacement medication regularly. Liotrix is a synthetic mix of levothyroxine (T4) and liothyronine (T3) in a 4:1 combination. Liotrix has a faster onset of action with a peak of 2 to 3 days, as opposed to levothyroxine, with a peak of 1 to 3 weeks.

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.” C

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 Management Nursing Diagnoses
Imbalanced nutrition: More than body requirements Activity intolerance Impaired memory

Nursing Management Planning
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. Administer thyroid hormone replacement therapy and all other medications IV because paralytic ileus may be present in the patient with myxedema coma.

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 Note energy level and mental alertness. These should increase within 2 to 14 days and should continue to rise steadily to normal levels.

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. Initially, the hypothyroid patient needs more time to comprehend all of the necessary information. It is important to provide written instructions, repeat the information often, and assess the patient’s comprehension level. Specifically, include in the teaching plan the signs and symptoms of hypothyroidism or hyperthyroidism that indicate hormone imbalance.

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 Management Evaluation
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

Discussion Questions What are some possible causes of her symptoms?
1. Depression, hypothyroidism, anemia, cardiac disease, F/E imbalance, and allergies

Discussion Questions 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? 2. She will need to take thyroid medication every day for the rest of her life, but this medication will manage her symptoms well.

Discussion Questions What teaching will you need to do with her before she leaves the clinic? 3. Discuss the signs of hyperthyroidism, so she can be aware if she develops them.

Goiter Table Drugs that are Goitrogens.

Thyroid Nodules and Cancer
Types of Thyroid Cancer Clinical Manifestations and Diagnostic Studies

Thyroid Nodules and Cancer
Fig A large “cold” nodule on the thyroid gland (arrow) detected by a scan.

Thyroiditis Fig Hashimoto’s thyroiditis.

Hyperthyroidism Etiology and Pathophysiology Clinical Manifestations
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 on Cushing Syndrome and Addison’s Disease

Disorders of the Adrenal Cortex Corticosteroids
Adrenal cortex steroid hormones Glucocorticoids Regulate metabolism and ↑ blood glucose Critical to physiologic stress response Mineralocorticoids regulate Sodium balance Potassium balance Cushing syndrome is a spectrum of clinical abnormalities caused by an excess of corticosteroids, particularly glucocorticoids. See Table for several conditions that can cause Cushing syndrome.

Disorders of the Adrenal Cortex Corticosteroids
Adrenal cortex steroid hormones Androgen contributes to Growth and development in both genders Sexual activity in adult women

Cushing Syndrome Etiology and Pathophysiology
Caused by excess of corticosteroids, particularly glucocorticoids Most common cause Iatrogenic administration of exogenous corticosteroids

Cushing Syndrome Table 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 Syndrome Clinical 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 See Table for clinical manifestations. Although manifestations of glucocorticoid excess usually predominate, symptoms of mineralocorticoid and androgen excess may also be seen. {See next 2 slides for figures.}

Facies include a rounded face (“moon face”) with thin, reddened skin. Hirsutism may also be present. Fig Cushing syndrome. Facies include a rounded face (“moon face”) with thin, reddened skin. Hirsutism may also be present.

Fig 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. C. Iatrogenic Cushing’s disease is Cushing’s disease caused by medical treatment --- In this case, by taking excessive steroids resulting in the symptoms of moon face, buffalo hump, and other associated symptoms.

Loss of collagen Wound healing delayed Mood disturbances Insomnia Irrationality Psychosis The loss of collagen makes the skin weaker and thinner, and therefore more easily bruised.

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 Overall, clinical manifestations of particular importance are (1) centripetal (truncal) obesity or generalized obesity; (2) “moon facies” (fullness of the face) with facial plethora; (3) purplish red striae (usually depressed below the skin surface) on the abdomen, breast, or buttocks; (4) hirsutism in women; (5) menstrual disorders in women; (6) hypertension; and (7) unexplained hypokalemia. {See next slide for figure.}

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

Cushing Syndrome Diagnostic 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 Examples of medication inducing false-positives include phenytoin (Dilantin) and rifampicin (Rifampin). Urine levels of 17-ketosteroids may be elevated.

Hypokalemia and alkalosis are seen in ectopic ACTH syndrome and adrenal carcinoma. Plasma ACTH may be low, normal, or elevated, depending on problem. High or normal ACTH levels indicate Cushing disease, whereas low or undetectable levels indicate an adrenal or medication cause.

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 Syndrome Collaborative 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 See Table for more information. Occasionally, bilateral adrenalectomy is necessary. Laparoscopic adrenalectomy is used unless a known or suspected malignant adrenal tumor is present. An open surgical adrenalectomy is used for adrenal cancer.

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. The best treatment for ectopic Cushing syndrome is surgical removal of the tumor. This is usually possible when the tumor is benign. However, many tumors are malignant and have metastasized before cortisol excess has been diagnosed. Surgical removal is not possible in these situations, and drugs to suppress cortisol secretion may be given. Drugs that are used include ketoconazole (Nizoral) and aminoglutethimide (Cytadren). These drugs are used cautiously because they are often toxic at doses needed to reduce corticosteroid synthesis.

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. An alternate-day regimen is one in which twice the daily dosage of a shorter-acting corticosteroid is given every other morning to minimize hypothalamic-pituitary-adrenal suppression, growth suppression, and altered appearance. This regimen is not used when the corticosteroids are given as hormone replacement.

Cushing Syndrome Nursing Assessment
Patient medical history Pituitary tumor Adrenal, pancreatic, or pulmonary neoplasms GI bleeding Frequent infections Subjective and objective data that should be obtained from a patient with Cushing syndrome are presented in Table

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 Syndrome Nursing Diagnoses
Risk for infection Imbalanced nutrition Disturbed body image Impaired skin integrity

Cushing Syndrome Nursing Planning
Patient goals include Experience relief of symptoms Have no serious complications Maintain positive self-image Actively participate in therapeutic plan

Cushing Syndrome Nursing 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 Because signs and symptoms of inflammation (e.g., fever, redness) may be minimal or absent, assess for pain, loss of function, and purulent drainage. Signs and symptoms of abnormal thromboembolic events include sudden chest pain, dyspnea, or tachypnea.

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. Changes in appearance such as centripetal obesity, multiple bruises, hirsutism in women, and gynecomastia in men can be distressing.

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 If large amounts of endogenous hormone have been released into the systemic circulation during surgery, the patient is likely to develop hypertension, increasing the risk of hemorrhage. High levels of corticosteroids also increase susceptibility to infection and delay wound healing.

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. IV corticosteroids are given, and the dose and rate of flow are adjusted to the patient’s clinical manifestations and fluid and electrolyte balance. Oral doses are given as tolerated.

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 The nurse should report these signs and symptoms so that drug doses can be adjusted as necessary.

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. A nursing care plan for the patient with Cushing syndrome is available on the Evolve website,

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. The nurse may consider a visiting nurse referral, especially for older adults, because of the need for ongoing evaluation and educational needs. Patients should be taught to adjust their corticosteroid replacement therapy in accordance with their stress levels.

Cushing Syndrome Nursing Evaluation
Expected outcomes Experience no signs or symptoms of infection. Attain weight appropriate for height. Increase acceptance of appearance. Maintain intact skin.

Question 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. Answer: 3 Rationale: Hydrocortisone is administered IV during and after a bilateral adrenalectomy to ensure adequate responses to the stress of the procedure.

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
What syndrome has he likely developed? What is the most probable cause of this change? What is his primary nursing management? Cushing syndrome. Use of oral steroids. Education about Cushing syndrome and the need to call his health care provider about changing his medications.

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? 4. Help him fill a weekly medication organizer with the medications.

Focus on Addison’s Disease

Addison’s Disease Etiology 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 In secondary adrenocortical insufficiency, corticosteroids and androgens are deficient, but mineralocorticoids rarely are. ACTH deficiency may be caused by pituitary disease or suppression of the hypothalamic-pituitary axis as a result of administration of exogenous corticosteroids.

Common cause is autoimmune response to adrenal tissue. Susceptibility genes beginning to be identified Other endocrine conditions often found When other endocrine conditions are present, Addison’s disease is considered a component of polyendocrine deficiency syndrome.

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 Disease Clinical 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 The manifestations have a very slow (insidious) onset. Skin hyperpigmentation, a striking feature, is seen primarily in sun-exposed areas of the body, at pressure points, over joints, and in the creases, especially palmar creases. {See next slide for figure.}

Hyperpigmentation It most likely is due to increased secretion of β-lipotropin (which contains melanocyte-stimulating hormone [MSH]) or ACTH. These tropic hormones are increased because of decreased negative feedback and subsequent low corticosteroid levels. Fig 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 Disease Complications
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 Hypotension is particularly postural.

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 Disease Diagnostic 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. A positive response to ACTH stimulation points to a probable diagnosis of pituitary disease.

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 See Table for more information.

Addison’s Disease Collaborative Care
Hydrocortisone Most commonly used as replacement therapy Glucocorticoid dosage must be ↑ during times of stress to prevent addisonian crisis. Hydrocortisone has both glucocorticoid and mineralocorticoid properties. Mineralocorticoid replacement with fludrocortisone (Florinef) is administered daily with increased salt in the diet.

Addison’s Disease Collaborative Care
Addisonian crisis Treatment directed at Shock management High-dose hydrocortisone replacement Large volumes of 0.9% saline solution and 5% dextrose are administered to reverse hypotension and electrolyte imbalances until BP returns to normal.

Addison’s Disease Nursing 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 The patient cannot cope with these extremes because of the inability to produce corticosteroids.

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 The serious nature of the disease and the need for lifelong replacement therapy necessitate a well-organized and carefully presented teaching plan. Table outlines the major areas that must be included in the teaching plan.

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. Minor stressor examples: Respiratory infection, dental work Major stressor examples: Divorce, loss of a parent If vomiting or diarrhea occurs, as may happen with influenza, the health care provider must be notified immediately because electrolyte replacement may be necessary. In addition, these manifestations may be early indicators of crisis.

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 Therapy Effects 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. See Table for more information.

Corticosteroid Therapy Effects of Corticosteroid Therapy
Expected effects of corticosteroid therapy Antiinflammatory action Immunosuppression Maintenance of normal BP Carbohydrate and protein metabolism A beneficial effect in one situation may be a harmful one in another. For example, the vasopressive effect of the hormone is critical in enabling the organism to function in stressful situations but can produce hypertension when used for drug therapy. Specific side effects related to corticosteroid therapy are listed in Table

Corticosteroid Therapy Management
Should be taken in the morning with food to reduce gastric irritation Must not be stopped abruptly Assess for corticosteroid-induced osteoporosis. Corticosteroids taken for >1 week will suppress adrenal production, and oral steroids should be tapered. Therapies to reduce the resorption of bone may include increased calcium intake, vitamin D supplementation, bisphosphonates (e.g., alendronate [Fosamax]), and institution of a low-impact exercise program.

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 Occasionally, multiple lesions are involved and are associated with bilateral adrenal hyperplasia. PA affects both genders equally and occurs most frequently between 30 and 50 years of age. It is estimated that approximately 1% of cases of hypertension are caused by PA.

Hyperaldosteronism Clinical Manifestations
Elevated levels of aldosterone Sodium retention Elimination of potassium Sodium retention leads to Hypernatremia Hypertension Headache Edema does not usually occur because the rate of sodium excretion increases, which prevents more severe sodium retention.

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. The diagnosis of hyperaldosteronism should be suspected in all hypertensive patients with hypokalemia who are not being treated with diuretics.

Hyperaldosteronism Treatment
Preferred treatment for primary hyperaldosteronism is surgical removal of the adenoma. Although this surgery can be done as an open procedure, laparoscopic adrenalectomy is most frequently performed because of the benefits that this minimally invasive surgery offers.

Hyperaldosteronism Treatment
Before surgery, patients need Low-sodium diet Potassium-sparing diuretics Antihypertensive agents Assess BP Fluid/electrolyte balance Potassium-sparing diuretics include spironolactone (Aldactone) and eplerenone (Inspra). Oral potassium supplements and sodium restrictions may also be necessary. BP must be monitored because unilateral adrenalectomy is successful in controlling hypertension in only 80% of patients with adenoma.

Pheochromocytoma Etiology and Pathophysiology
Caused by a tumor of the adrenal medulla Produces excessive catecholamines Most often in young to middle-aged adults The most dangerous immediate effect of the disease is severe hypertension. If left untreated, it may lead to hypertensive encephalopathy, diabetes mellitus, cardiomyopathy, and death.

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. Attacks may be provoked by many medications, including antihypertensives, opioids, radiologic contrast media, and tricyclic antidepressants. The duration of the attacks may vary from a few minutes to several hours. Pheochromocytoma is an uncommon cause of hypertension, accounting for only 0.1% of all cases of hypertension. Consider this condition in patients who do not respond to traditional hypertensive treatments.

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 Treatment with α-adrenergic and β-blockers is required preoperatively to control blood pressure and prevent intraoperative hypertensive crises. After adequate α-adrenergic blockade, β-blockers (e.g., propranolol [Inderal]) are used to decrease tachycardia and other dysrhythmias.

Monitor BP closely. Make patient as comfortable as possible. Monitor glucose. Preoperative and postoperative care is similar to that for any patient undergoing adrenalectomy, except that BP fluctuations from catecholamine excesses tend to be severe and must be carefully monitored.

Patient needs Rest Nourishment Emotional support Stress importance of Follow-up care Routine BP monitoring

Question 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. Answer: 1 Rationale: The patient in acute adrenal insufficiency will have the following clinical manifestations: Hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, and confusion. Collaborative care will include administration of corticosteroids. An outcome that would indicate patient improvement would be improved level of consciousness (i.e., alert and oriented).

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

Based on the findings, what are her possible diagnoses? What is her primary acute nursing management? Addison’s disease. Frequent nursing assessment and protection from extremes.

What critical patient teaching should you do with her about her home care? What lifestyle modifications should she make? 3. Discuss the serious nature of the disease and the need for lifelong replacement therapy (see Table for major areas that must be included in the teaching plan). 4. Always carry an emergency kit.

Nursing Management: Endocrine Problems

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