Nursing Management: - PowerPoint Presentation

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

Disorders of the AnteriorAcromegalyGigantismHypopituitarismDwarfism

Acromegaly Etiology and PathophysiologyOverproduction of growth hormone (Usually caused by benign pituitary tumor (adenoma)Clinical ManifestationsDepends on age

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

Acromegaly Diagnostic StudiesHistory and physicalEvaluation of plasma insulin (OGGT)MRI and CTCollaborative Care Surgical therapy

Acromegaly Fig. 50-2. 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.

QuestionFollowing a hypophysectomy for acromegaly, postoperative nursing care should focus onA. 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, continuedRadiation therapyDrug therapySandostatin

Nursing Management: Acromegaly Nursing Assessments/s of abnormal issue growth and evaluate changes in size of patientLike What?Nursing Implementation Post operative hypophysectomy Life long hormone replacement therapy Assess for DI because of possible damage to posterior lobe

Hypofunction of Pituitary GlandEtiology and PathophysiologyTumorAutoimmune disorderInfectionPituitary infarction (Sheehan s yndrome) 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 GlandTumor removal with lifelong hormone replacement therapy

Disorders of Posterior Pituitary GlandSIADH (syndrome of inappropriate diuretic hormone)Over production of ADHDI (Diabetes Insipidus)Underproduction of ADH

Syndrome of Inappropriate Antidiuretic HormoneEtiology and PathophysiologyAbnormal production of ADHTumor CNS disorderDrug therapyCentral nervous system disorders Miscellaneous conditions See table 50-1 page 1259

Syndrome of Inappropriate Antidiuretic Hormone Fig. 50-3. Pathophysiology of syndrome of inappropriate antidiuretic hormone (SIADH).

Syndrome of Inappropriate Antidiuretic HormoneClinical Manifestations and Diagnostic StudiesFluid overloadHyponatremiaLow urine output Cerebral edema Seizures and coma Diagnostic Studies Serum sodium < 134 Serum osmolality < 280 Urine specific gravity > 1.005

Nursing and Collaborative Management: Syndrome of Inappropriate Antidiuretic HormoneTreat underlying causeFluid restrictionHypertonic saline (slow infusion rateLop diuretics with supplements of K+, Ca+, Mg++ Declomycin (blocks ADH Vasopressin receptor antagonists

QuestionA patient with a head injury develops SIADH. Symptoms the nurse would expect to find includeA. 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 PathophysiologyDeficiency of ADHResults in fluid and electrolyte lossNeurogenicNephrogenic (lithium most common cause) Psychogenic (excessive water intake)

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

Diabetes Insipidus Clinical ManifestationsPolydipsia Polyuria 5-20L/dayLow specific gravitySerum 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 causeReplace fluids and electrolytesHormone 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.

HyperthyroidismA sustained increase in synthesis and release of thyroid hormones by thyroid glandOccurs more often in women Highest frequency in 20- to 40-year-olds

HyperthyroidismMost common form Graves’ disease Other causes Thyroiditis Toxic nodular goiter Exogenous iodine excess Pituitary tumors Thyroid cancer

HyperthyroidismThyrotoxicosisPhysiologic effects/clinical syndrome of hypermetabolism resulting from increased circulating levels of T 3 , T 4 Hyperthyroidism and thyrotoxicosis occur together as Graves’ disease.

Etiology and PathophysiologyGraves’ diseaseAutoimmune disease of unknown origin Diffuse thyroid enlargement Excessive thyroid hormone secretion

Etiology and PathophysiologyGraves’ disease (cont’d)Precipitating factors Insufficient iodine supply Infection Stressful life events interacting with genetic factors Accounts for 75% of cases of hyperthyroidism

Etiology and PathophysiologyGraves’ disease (cont’d)Antibodies are developed to TSH receptor. Leads to clinical manifestations of thyrotoxicosis May progress to destruction of thyroid tissue, causing hypothyroidism

Etiology and PathophysiologyToxic 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 ManifestationsRelated to effect of thyroid hormone excess↑ metabolism ↑ tissue sensitivity to stimulation by sympathetic nervous system

Clinical ManifestationsOphthalmopathyAbnormal 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.

Clinical ManifestationsCardiovascular systemBruit over thyroid gland Systolic hypertension ↑ cardiac output Dysrhythmias Cardiac hypertrophy Atrial fibrillation

Clinical ManifestationsGI system↑ appetite, thirst Weight loss Diarrhea Splenomegaly Hepatomegaly

Clinical ManifestationsIntegumentary systemWarm, 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.

Clinical ManifestationsMusculoskeletal systemFatigue Muscle weakness Proximal muscle wasting Dependent edema Osteoporosis

Clinical ManifestationsNervous systemFine tremors Insomnia Ability of mood, delirium Hyperreflexia of tendon reflexes Inability to concentrate

Clinical ManifestationsReproductive systemMenstrual irregularities Amenorrhea Decreased libido Impotence Gynecomastia in men Decreased fertility

Clinical ManifestationsIntolerance to heat↑ sensitivity to stimulant drugs Elevated basal temperature

ComplicationsThyrotoxic crisisAcute, rare condition, where all manifestations are heightened Life-threatening emergency Death rare when treatment initiated Presumed causes are additional stressors.

ComplicationsThyrotoxic crisisManifestations include Tachycardia Heart failure Shock Hyperthermia Restlessness

ComplicationsThyrotoxic crisisManifestations (cont’d) Agitation Seizures Abdominal pain Nausea

ComplicationsThyrotoxic crisisManifestations (cont’d) Vomiting Diarrhea Delirium Coma

ComplicationsThyrotoxic crisisTreatment ↓ Thyroid hormone levels and clinical manifestations with drug therapy Therapy Aimed at managing respiratory distress, fever reduction, fluid replacement, and management of stressors

Diagnostic StudiesHistoryPhysical examination Ophthalmologic examination ECG Radioactive iodine uptake (RAIU) Indicated to differentiate Graves’ disease from other forms of thyroiditis

Diagnostic StudiesLaboratory testsTSH Free thyroxine (free T4) Total T3 and T4

Collaborative CareGoalsBlock adverse effects of thyroid hormones. Stop hormone oversecretion.

Collaborative CareThree primary treatment optionsAntithyroid medications Radioactive iodine therapy (RAI) Subtotal thyroidectomy

Collaborative CareDrug therapyUseful in treatment of thyrotoxic states Not considered curative Antithyroid drugs Iodine β -adrenergic blockers

Collaborative CareAntithyroid drugsInhibit synthesis of thyroid hormone Improvement in 1 to 2 weeks Good results in 4 to 8 weeks Therapy for 6 to 15 months

Collaborative CareAntithyroid 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 CareIodine 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 CareIodine (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 Careβ-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 CareRadioactive 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 CareRAI (cont’d)High incidence of posttreatment hypothyroidism Need for lifelong thyroid hormone replacement

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

Collaborative CareSurgical therapy (cont’d)Subtotal thyroidectomy Preferred surgical procedure Involves removal of significant portion of thyroid 90% removed to be effective

Collaborative CareSurgical therapy (cont’d)Endoscopic thyroidectomy appropriate with small nodules and no malignancy Less scarring, pain, and recovery time

Collaborative CareSurgical therapy (cont’d)Before surgery Antithyroid drugs, iodine, and β -adrenergic blockers may be administered To achieve euthyroid state To control symptoms

Collaborative CareNutritional therapyHigh-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 AssessmentHealth history Preexisting goiter Recent infection or trauma Immigration from iodine-deficient area Medications Family history of thyroid or autoimmune disorders

Nursing ManagementNursing AssessmentWeight loss Nausea Diarrhea Dyspnea on exertion Muscle weakness Insomnia Heat intolerance

Nursing ManagementNursing AssessmentDecreased libido Impotence Amenorrhea Irritability Personality changes Delirium

Nursing ManagementNursing AssessmentObjective Data Agitation Hyperthermia Enlarged or nodular thyroid gland Eyelid retraction Diaphoretic skin

Nursing ManagementNursing AssessmentBrittle nails Edema Tachypnea Tachycardia Hepatosplenomegaly

Nursing ManagementNursing AssessmentHyperreflexia Fine tremors Muscle wasting Coma Menstrual irregularities Infertility

Nursing ManagementNursing DiagnosesActivity intolerance Risk for injury Imbalanced nutrition: Less than body requirements Anxiety Insomnia

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

Nursing ManagementNursing ImplementationAcute intervention Usually treated in outpatient setting Those with acute thyrotoxicosis or undergoing thyroidectomy require hospitalization and acute care.

Nursing ManagementNursing ImplementationAcute thyrotoxicosis Requires aggressive treatment Administer medications to block thyroid hormone production. Administer IV fluids. Ensure adequate oxygenation.

Nursing ManagementNursing ImplementationAcute thyrotoxicosis (cont’d) Calm, quiet room Cool room Light bed coverings

Nursing ManagementNursing ImplementationAcute 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.

Nursing ManagementNursing ImplementationAcute 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.

Nursing ManagementNursing ImplementationThyroid 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.

Nursing ManagementNursing ImplementationThyroid 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

Nursing ManagementNursing ImplementationThyroid 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

Nursing ManagementNursing ImplementationThyroid 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.

Nursing ManagementNursing ImplementationAmbulatory 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.

Nursing ManagementNursing ImplementationAmbulatory 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 ManagementEvaluationRelief 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 84

Case Study28-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 StudyShe also claims to always be tired. Her skin is warm and moist. Her nails have become brittle.

Case StudyShe has a bounding pulse and a slight heart murmur. Palpation of her thyroid reveals a nodular goiter.

Case StudyLabs reveal↓ TSH↑ free thyroxine (free T4)

Discussion QuestionsWhat problem do her symptoms and lab values suggest? What treatments may the patient require?

Discussion QuestionsWhat follow-up will she need with these treatments? What important patient teaching should you do following these treatments?

HypothyroidismOne of the most common medical disorders in the United StatesAffects 1 in 50 women and 1 in 300 men

Etiology and PathophysiologyResults from insufficient circulating thyroid hormoneResult of a variety of abnormalities

Etiology and PathophysiologyCan be primary or secondaryPrimary Related to destruction of thyroid tissue or defective hormone synthesis Secondary Related to pituitary disease with ↓ TSH secretion or hypothalamic dysfunction

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Etiology and PathophysiologyMay be transient, related to thyroiditis, or result from discontinuing thyroid hormone therapy

Etiology and PathophysiologyIodine 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.

Etiology and PathophysiologyMay also develop because of treatment for hyperthyroidismAmiodarone and lithium can produce hypothyroidism.

Etiology and PathophysiologyCretinism is caused by thyroid hormone deficiencies during fetal or neonatal life.All infants are screened at birth for ↓ thyroid function.

Clinical ManifestationsVary depending on Severity Duration Age of onset Systemic effects characterized by slowing of body processes

Clinical ManifestationsRanges from no symptoms to classic symptoms and physical changes easily detected on examination

Clinical ManifestationsOnset of symptoms may occur over months to years.Unless occurs after thyroidectomy, thyroid ablation, treatment with antithyroid drugs

Clinical ManifestationsCardiovascular system↓ cardiac output ↓ cardiac contractility Anemia Cobalamin, iron, folate deficiencies ↑ serum cholesterol and triglycerides

Clinical ManifestationsRespiratory systemLow exercise tolerance Shortness of breath on exertion

Clinical ManifestationsNeurologic systemFatigued and lethargic Personality and mood changes Impaired memory, slowed speech, decreased initiative, and somnolence

Clinical ManifestationsGastrointestinal system↓ motility Achlorhydria Constipation

Clinical ManifestationsOther changesCold intolerance Hair loss Dry/coarse skin Brittle nails Hoarseness Muscle weakness and swelling Weight gain Menorrhagia

Clinical ManifestationsThose 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; and prominent tongue.

ComplicationsMental sluggishnessDrowsiness Lethargy progressing gradually or suddenly to impairment of consciousness or coma Myxedema coma

Diagnostic StudiesHistory and physical examinationLaboratory tests Serum TSH Determines cause of hypothyroidism Free T4 Serum T3 Serum T4

Diagnostic StudiesLaboratory findings (cont’d)Other abnormal findings are ↑ cholesterol and triglycerides, anemia, and ↑ creatine kinase.

Diagnostic StudiesTRH stimulation test↑ in TSH after TRH injection suggests hypothalamic dysfunction. No change after TRH injection suggests anterior pituitary dysfunction.

Collaborative CareRestoration of euthyroid state as safely and rapidly as possibleLow-calorie diet

Collaborative CareLevothyroxine (Synthroid)Must take regularly Monitor for angina and cardiac dysrhythmias. Monitor thyroid hormone levels, and adjust (as needed). Liotrix (Thyrolar)

QuestionThe 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.”

Nursing ManagementNursing Assessment Health history Weight gain Mental changes Fatigue Slowed/slurred speech Cold intolerance Skin changes

Nursing ManagementNursing AssessmentHealth history (cont’d) Constipation Dyspnea Recent introduction of iodine medications

Nursing ManagementNursing Assessment Physical examination Bradycardia Distended abdomen Dry, thick, cold skin Thick, brittle nails Paresthesias Muscular aches and pains

Nursing ManagementNursing DiagnosesImbalanced nutrition: More than body requirements Activity intolerance Impaired memory

Nursing ManagementPlanningExperience relief of symptoms. Maintain a euthyroid state. Maintain a positive self-image. Comply with lifelong thyroid replacement therapy.

Nursing ManagementNursing ImplementationHealth 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

Nursing ManagementNursing ImplementationAcute intervention Most individuals do not require acute nursing care. Managed on outpatient basis

Nursing ManagementNursing ImplementationAcute 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.

Nursing ManagementNursing ImplementationAcute intervention (cont’d) Individual with myxedema coma (cont’d) Vital signs Weight I & O Visible edema Cardiovascular response to hormone Energy level Mental alertness

Nursing ManagementNursing ImplementationAmbulatory 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.

Nursing ManagementNursing ImplementationAmbulatory 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.

Nursing ManagementNursing ImplementationAmbulatory and home care (cont’d) Discuss measures to minimize constipation. Avoid enemas because of vagal stimulation in cardiac patient.

Nursing ManagementNursing ImplementationAmbulatory and home care (cont’d) Teach patient to notify physician immediately if signs of overdose appear. Orthopnea, dyspnea, rapid pulse, palpitations, nervousness, insomnia

Nursing ManagementNursing ImplementationAmbulatory and home care (cont’d) Patient with diabetes should test capillary blood glucose at least daily. Return to euthyroid state frequently. ↑ insulin requirements.

Nursing ManagementNursing ImplementationAmbulatory 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

Nursing ManagementNursing ImplementationAmbulatory and home care (cont’d) Provide handouts that include verbal instructions for patients and family members.

Nursing ManagementEvaluationExpected 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 Study38-year-old woman enters a community outpatient clinic. She is complaining of overwhelming fatigue that is not relieved by rest.

Case StudyShe 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 StudyHer face is puffy, and her skin is dry and pale. She is dressed inappropriately for warm weather.

Case StudyShe also complains of generalized body aches and pains with frequent muscle cramps and constipation.

Case StudyVital signsBP 142/84Heart rate 52 Respiratory rate 12 Temperature 96.8° F

Discussion QuestionsWhat are some possible causes of her symptoms?

Discussion QuestionsNo 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?

Discussion QuestionsWhat teaching will you need to do with her before she leaves the clinic?

Goiter Table 50-4. Drugs that are Goitrogens.

Thyroid Nodules and CancerTypes of Thyroid CancerClinical 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 PathophysiologyGraves’ diseaseToxic nodular goitersClinical Manifestations

Hyperthyroidism ComplicationsDiagnostic Studies

Hyperthyroidism Collaborative Care Drug therapyAntithyroid drugsIodineΒ ‑adrenergic blockers Radioactive iodine therapy Surgical therapy Nutritional therapy

Nursing Management: Hyperthyroidism Nursing Assessment Nursing DiagnosesPlanning

Nursing Management: Hyperthyroidism Nursing ImplementationAcute interventionAcute thyrotoxicosis Thyroid surgery Ambulatory and home care Postoperative care Evaluation

Hypothyroidism Etiology and PathophysiologyClinical Manifestations

Disorders of Parathyroid Glands

Hyperparathyroidism Etiology and PathophysiologyPrimary or secondaryClinical Manifestations and ComplicationsDiagnostic Studies Serum calcium (high)and phosphorus levels (low) Bone x-rays and bone density tests Collaborative Care Surgical therapy Nonsurgical therapy

Nursing Management:Hyperparathyroidism ParathyroidectomySimilar to that of thyroidectomy

HypoparathyroidismUsually due to removal of parathyroid gland(iatrogenic)

Nursing and Collaborative Management:HypoparathyroidismGive 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 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.

Cushing SyndromeEtiology and Pathophysiology 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 SyndromeEtiology and Pathophysiology 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

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

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

Cushing SyndromeClinical Manifestations Hyperglycemia Glucose intolerance associated with cortisol-induced insulin resistance Increased gluconeogenesis by liver

Cushing SyndromeClinical ManifestationsProtein wasting Catabolic effects of cortisol Leads to weakness, especially in extremities Protein loss in bones leads to osteoporosis, bone and back pain.

QuestionWhich 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.

Cushing SyndromeClinical Manifestations Loss of collagen Wound healing delayed Mood disturbances Insomnia Irrationality Psychosis

Cushing SyndromeClinical Manifestations Mineralocorticoid excess may cause hypertension secondary to fluid retention. Adrenal androgen excess may cause Pronounced acne Virilization in women Feminization in men

Cushing SyndromeClinical Manifestations Seen more commonly in adrenal carcinomas Women: Menstrual disorders and hirsutism Men: Gynecomastia and impotence Purplish red striae on abdomen, breast, or buttocks

Cushing SyndromeClinical Manifestations 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

Cushing SyndromeDiagnostic Studies 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

Cushing SyndromeDiagnostic Studies Hypokalemia and alkalosis are seen in ectopic ACTH syndrome and adrenal carcinoma. Plasma ACTH may be low, normal, or elevated, depending on problem.

Cushing SyndromeDiagnostic Studies Associated findings that are not diagnostic of Cushing syndrome Leukocytosis Lymphopenia Eosinopenia Hyperglycemia

Cushing SyndromeDiagnostic Studies 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

Cushing SyndromeCollaborative Care 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.

Cushing SyndromeCollaborative Care 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

Cushing SyndromeNursing Assessment Use of corticosteroids Weight gain Anorexia Polyuria Prolonged wound healing Weakness, fatigue

Cushing SyndromeNursing Assessment Easy bruising Insomnia Headache, back, joint, bone, and rib pain Amenorrhea Impotence

Cushing SyndromeNursing Assessment Mood disturbances, anxiety, psychosis, poor concentration Truncal obesity Buffalo hump Moon face Hirsutism of body and face

Cushing SyndromeNursing Assessment Thinning of head hair Thin, friable skin Acne Petechiae Purpura Hyperpigmentation

Cushing SyndromeNursing Assessment 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.

Cushing SyndromeNursing Implementation Acute intervention Assessment of Signs and symptoms of hormone and drug toxicity Complicating conditions Cardiovascular disease Diabetes mellitus Infection

Cushing SyndromeNursing Implementation Acute intervention (cont’d) Monitor Vital signs Daily weight Glucose Infection Signs and symptoms of abnormal thromboembolic phenomena

Cushing SyndromeNursing Implementation 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.

Cushing SyndromeNursing Implementation Preoperative care Patient should be in optimal physical condition. Control hypertension and hyperglycemia. Hypokalemia must be corrected with diet and potassium supplements.

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

Cushing SyndromeNursing Implementation Preoperative care (cont’d) Include information on postoperative care. Nasogastric tube Urinary catheter IV therapy Central venous pressure monitoring Leg compression devices

Cushing SyndromeNursing Implementation 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.

Cushing SyndromeNursing Implementation 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

Cushing SyndromeNursing Implementation 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.

Cushing SyndromeNursing Implementation Postoperative care (cont’d) Adrenal insufficiency develops if corticosteroid dosage is tapered rapidly. Indications of hypocortisolism Vomiting Increased weakness Dehydration Hypotension

Cushing SyndromeNursing Implementation Postoperative care (cont’d) Patient may complain of Painful joints Pruritus Peeling skin Severe emotional disturbances

Cushing SyndromeNursing Implementation 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.

Cushing SyndromeNursing Implementation 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 What syndrome has he likely developed? What is the most probable cause of this change? What is his primary nursing management?

Case Study Discussion QuestionsCushing 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

Addison’s DiseaseEtiology and Pathophysiology All three classes of adrenal corticosteroids are ↓ in Addison’s disease. Glucocorticoids Mineralocorticoids Androgens

Addison’s DiseaseEtiology and Pathophysiology Common cause is autoimmune response to adrenal tissue. Susceptibility genes beginning to be identified Other endocrine conditions often found

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

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

Addison’s DiseaseEtiology and Pathophysiology 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

Addison’s DiseaseClinical Manifestations Primary features Progressive weakness Fatigue Weight loss Anorexia Skin hyperpigmentation

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

Addison’s DiseaseClinical Manifestations Orthostatic hypotension Hyponatremia Hyperkalemia Nausea and vomiting Diarrhea Irritability, depression

Addison’s DiseaseClinical Manifestations 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

Addison’s DiseaseComplications Severe manifestations of glucocorticosteroid and mineralocorticoid deficiencies Hypotension Tachycardia Dehydration Hyponatremia

Addison’s DiseaseComplications Manifestations (cont’d) Hyperkalemia Hypoglycemia Fever Weakness Confusion

Addison’s DiseaseComplications 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.

Addison’s DiseaseDiagnostic Studies Abnormal laboratory findings Hyperkalemia Hypochloremia Hyponatremia Hypoglycemia

Addison’s DiseaseDiagnostic Studies Abnormal laboratory findings (cont’d) Anemia ↑ BUN Low urine cortisol levels

Addison’s DiseaseDiagnostic Studies 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.

Addison’s DiseaseNursing Implementation Acute intervention (cont’d) Protect against infection. Assist with daily hygiene. Protect from extremes. Light Noise Temperature

Addison’s DiseaseNursing Implementation 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

Addison’s DiseaseNursing Implementation Ambulatory and home care (cont’d) Long-term care includes need for Extra medication Stress management

Addison’s DiseaseNursing Implementation Ambulatory and home care (cont’d) Situations requiring corticosteroid dose adjustment include Fever Influenza Tooth extraction Physical exertion

Addison’s DiseaseNursing Implementation 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 .

Addison’s DiseaseNursing Implementation 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

Hyperaldosteronism Clinical Manifestations Eliminating potassium leads to Hypokalemia Muscle weakness Fatigue Cardiac dysrhythmias

Hyperaldosteronism Clinical Manifestations 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 PheochrocytomaHeadaches (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 Pheochromoctyoma24 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

Pheochromocytoma Treatment Monitor BP closely. Make patient as comfortable as possible. Monitor glucose.

Pheochromocytoma Treatment 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

Case Study Discussion Questions Based on the findings, what are her possible diagnoses? What is her primary acute nursing management?

Case Study Discussion Questions What critical patient teaching should you do with her about her home care? What lifestyle modifications should she make?