Learning Objectives:At the end of this lecture, you will be able to:1. Describe the functions of each of the endocrineglands and their hormones.2. Identify the diagnostic tests used to determinealterations in function of each of the endocrineglands.3. Compare hypothyroidism and hyperthyroidism: theircauses, clinical manifestations, management, andnursing interventions.JOFRED M. MARTINEZ, RN
Learning Objectives:At the end of this lecture, you will be able to:4. Develop a plan of nursing care for the patientundergoing thyroidectomy.5. Compare hyperparathyroidism & hypoparathyroidismtheir causes, clinical manifestations, management,and nursing interventions.6. Compare Addison’s disease with Cushing’ssyndrome: their causes, clinical manifestations,management, and nursing interventions.7. Use the nursing process as a framework for care ofpatients with adrenal insufficiency.
Learning Objectives:At the end of this lecture, you will be able to:8. Use the nursing process as a framework for care ofpatients with Cushing’s syndrome.9. Identify the teaching needs of patients requiringcorticosteroid therapy.
Hormones• chemical substances secreted by the endocrineglands.• help to regulate organ function in relation withthe nervous system• mechanism for regulating hormoneconcentration in the bloodstream is callednegative feedback
Chemistry of HormonesHormones are classified into three groups:1. AMINES - structural variations of the aminoacid tyrosine.e.g. thyroxine from the thyroid gland and epinephrineand norepinephrine from the adrenal medulla2. PROTEINS - these hormones are chains ofamino acids.e.g. insulin from the pancreas, growth hormone fromthe anterior pituitary gland, and calcitonin from thethyroid gland
Chemistry of Hormones3. STEROIDS - cholesterol is the precursor forthe steroid hormonese.g. cortisol and aldosterone from the adrenal cortex,estrogen and progesterone from the ovaries, andtestosterone from the testes.
Work of Hormones1. HORMONAL MECHANISMThe hypothalamus secretes hormones thatstimulate the anterior pituitary gland to secretehormones that stimulate other endocrineglands to secrete hormones.
Work of Hormones2. HUMORAL MECHANISMCapillary blood contains a low concentration ofcalcium that stimulates secretion of parathyroidhormone.3. NEURAL MECHANISMPreganglionic SNS fiber stimulates the adrenalmedulla cells to secrete catecholamines.
Pituitary Gland• The pituitary gland, or the hypophysis, is around structure about 1.27 cm (1⁄2 inch) indiameter located on the inferior aspect of thebrain.• It is divided into the anterior, intermediate, andposterior lobes.• Commonly referred to as the master gland, thepituitary secretes hormones that control thesecretion of hormones by other endocrineglands
Major Actions and Source of HormonesANTERIOR PITUITARY1. Growth hormone (GH)• Stimulates growth of bone and muscle, promotesprotein synthesis and fat metabolism, decreasescarbohydrate metabolism2. Adrenocorticotropic hormone (ACTH)• Stimulates synthesis and secretion of adrenal corticalhormones3. Thyroid-stimulating hormone (TSH)• Stimulates synthesis and secretion of thyroid hormone
Major Actions and Source of HormonesANTERIOR PITUITARY4. Follicle-stimulating hormone (FSH)• Female: stimulates growth of ovarian follicle, ovulation• Male: stimulates sperm production5. Luteinizing hormone (LH)• Female: stimulates development of corpus luteum,release of oocyte, production of estrogen andprogesterone• Male: stimulates secretion of testosterone,development of interstitial tissue of testes
Major Actions and Source of HormonesPOSTERIOR PITUITARY1. Antidiuretic hormone (ADH)• Increases water reabsorption by kidney2. Oxytocin• Stimulates contraction of pregnant uterus, milkejection from breasts after childbirthIf you are a breast-feeding mom, hearing yourbaby cry, thinking about your baby, or smellingyour baby can cause the letdown reflex to occur.
HypopituitarismHYPOPITUITARISM• results from disease of the pituitary gland itselfor of the hypothalamus• results from destruction of the anterior lobe ofthe pituitary glandPanhypopituitarism (Simmonds’ disease) is totalabsence of all pituitary secretions.Postpartum pituitary necrosis (Sheehan’ssyndrome) is another uncommon cause of failure ofthe anterior pituitary.
HypopituitarismHypopituitarism is also a complication of:• radiation therapy to the head and neck area• total destruction of the pituitary gland bytrauma, tumor, or vascular lesion that removesall stimuli that are normally received by thethyroid, the gonads, and the adrenal glands.
HypopituitarismThe result of hypopituitarism is: Extreme weight loss Emaciation Hair loss Impotence Amenorrhea Hypometabolism Hypoglycemia Atrophy of all endocrine glands and organsComa and death occur if the missing hormones arenot replaced.
Pituitary Tumors• Pituitary tumors are usually benign, althoughtheir location and effects on hormoneproduction by target organs can cause lifethreatening effects.• Three principal types of pituitary tumors isrepresented by an overgrowth of: eosinophilic cells basophilic cells chromophobic cells
Pituitary Tumors (Manifestations)• Eosinophilic tumors that develop early in liferesult in GIGANTISM.• Basophilic tumors give rise to CUSHING’SSYNDROME with features largely attributableto hyperadrenalism, including masculinizationand amenorrhea in females, truncal obesity,hypertension, osteoporosis, and polycythemia.• Chromophobic tumors usually produce nohormones but destroy the rest of the pituitarygland, causing HYPOPITUITARISM.
Assessment and Diagnostic Findings• COMPUTED TOMOGRAPHY (CT) andMAGNETIC RESONANCE IMAGING (MRI)are used to diagnose the presence and extentof pituitary tumors.• Serum levels of pituitary hormones may beobtained along with measurements ofhormones of target organs (eg, thyroid,adrenal) to assist in diagnosis if otherinformation is inconclusive.
Medical / Surgical Management• Surgical removal of the pituitary tumor through atranssphenoidal approach is the usual treatment.• STEREOTACTIC RADIATION THERAPY, whichrequires use of a neurosurgery-type stereotacticframe, may be used to deliver external-beamradiation.• Other treatments include conventional radiationtherapy, bromocriptine (dopamine antagonist), andoctreotide (synthetic analog of growth hormone).
Medical / Surgical Management• HYPOPHYSECTOMY, or removal of the pituitarygland, is the treatment of choice in patients withCushing’s syndrome due to excessive productionof ACTH by a tumor of the pituitary gland.• Menstruation ceases and infertility occurs aftertotal or near-total ablation of the pituitary gland.Replacement therapy with CORTICOSTEROIDSand THYROID HORMONE is necessary.
• Diabetes insipidus is a disorder of the posterior lobe ofthe pituitary gland characterized by a deficiency ofantidiuretic hormone (ADH), or vasopressin.• Great thirst (polydipsia) and large volumes of diluteurine characterize the disorder.• It may be secondary to head trauma, brain tumor,infections of the central nervous system, tumors orsurgical ablation or irradiation of the pituitary gland.Diabetes insipidus (DI) has nothing to do withblood sugar. Diabetes mellitus (DM) haseverything to do with blood sugar.Diabetes Insipidus
Diabetes Insipidus• Another cause of diabetes insipidus is failure ofthe renal tubules to respond to ADH; thisnephrogenic form may be related tohypokalemia, hypercalcemia, and a variety ofmedications (eg, lithium).The only electrolyte that is affected by the amountof water in the vascular space is sodium. If thewater level in the blood is too high, the sodiumlevel will go down. If the water level in the blood istoo low, the sodium level will go up.
Diabetes Insipidus (Manifestations)• enormous daily output of very dilute, water-like urine specific gravity of 1.001 to 1.005 contains no abnormal substances such as glucoseand albumin• intense thirst, the patient tends to drink 2 to 20 litersof fluid daily and craves cold water.Attempts to restrict fluids cause the patient toexperience an insatiable craving for fluid and todevelop hypernatremia and severe dehydration.
Assessment and Diagnostic Finding• The FLUID DEPRIVATION TEST is carried out bywithholding fluids for 8 to 12 hours or until 3% to 5%of the body weight is lost. The patient is weighedfrequently during the test. Plasma and urineosmolality studies are performed at the beginningand end of the test.• Concurrent measurements of plasma levels of ADH(vasopressin) and plasma and urine osmolality, atrial of DESMOPRESSIN (synthetic vasopressin)therapy and intravenous infusion of hypertonic salinesolution.
Medical ManagementThe objectives of therapy are:1. To replace ADH (which is usually a long-termtherapeutic program)2. To ensure adequate fluid replacement3. To identify and correct the underlying intracranialpathology.
Pharmacologic Management• DESMOPRESSIN (DDAVP), is administeredintranasally; the patient sprays the solution into thenose through a flexible calibrated plastic tube. Oneor two administrations daily or every 12 to 24 hoursusually control the symptoms.• Intramuscular administration of ADH, orVASOPRESSIN TANNATE IN OIL. It is administeredevery 24 to 96 hours. The vial of medication shouldbe warmed or shaken vigorously beforeadministration. The injection is administered in theevening so that maximum results are obtainedduring sleep.
Pharmacologic Management• Clofibrate, a hypolipidemic agent, given on patientswith diabetes insipidus who have some residualhypothalamic vasopressin.• Chlorpropamide (Diabinese) and thiazide diureticsare also used in mild forms of the disease becausethey potentiate the action of vasopressin.The patient receiving chlorpropamide should bewarned of the possibility of hypoglycemicreactions.
Nursing Management• Provide encouragement and support while the patient isundergoing studies for a possible cranial lesion.• Inform the patient and family about follow-up care andemergency measures.• Provide specific verbal and written instructions, show thepatient how to administer the medications, and observereturn demonstrations as appropriate.• Advise the patient to wear a medical identificationbracelet and to carry medication and information aboutthis disorder at all times.Vasopressin must be administered with caution if thepatient has coronary artery disease because themedication causes vasoconstriction.
Syndrome of Inappropriate ADH• SYNDROME OF INAPPROPRIATE ANTIDIURETICHORMONE (SIADH) secretion includes excessivegrowth hormone (ADH) secretion from the pituitarygland even in the face of subnormal serumosmolality.• Patients with this disorder cannot excrete a diluteurine. They retain fluids and develop a sodiumdeficiency known DILUTIONAL HYPONATREMIA.
SIADH• Disorders of the central nervous system, such ashead injury, brain surgery or tumor, and infection, arethought to produce SIADH by direct stimulation ofthe pituitary gland.• Some medications (vincristine, phenothiazines,tricyclic antidepressants, thiazide diuretics, andothers) and nicotine have been implicated in SIADH;they either directly stimulate the pituitary gland orincrease the sensitivity of renal tubules to circulatingADH.
Medical Management• Eliminating the underlying cause, if possible, andrestricting fluid intake.• Diuretics (eg, furosemide [Lasix]) may be used alongwith fluid restriction if severe hyponatremia ispresent.• Close monitoring of fluid intake and output, dailyweight, urine and blood chemistries, and neurologicstatus• Supportive measures and explanations ofprocedures and treatments assist the patient to dealwith this disorder
Medical Management• Eliminating the underlying cause, if possible, andrestricting fluid intake.• Diuretics (eg, furosemide [Lasix]) may be used alongwith fluid restriction if severe hyponatremia ispresent.• Close monitoring of fluid intake and output, dailyweight, urine and blood chemistries, and neurologicstatus• Supportive measures and explanations ofprocedures and treatments assist the patient to dealwith this disorder
Anatomy & Physiology• butterfly-shaped organ consists of two laterallobes connected by an isthmus located in thelower neck anterior to the trachea• about 5 cm long and 3 cm wide and weighsabout 30 g• blood flow to the thyroid is very high (about 5mL/min per gram of thyroid tissue), about fivetimes the blood flow to the liver
Major Actions and Source of HormonesTHYROID (FOLLICULAR CELLS)Thyroid hormones:1. Triiodothyronine (T3)2. Thyroxine (T4)• Increase the metabolic rate; increase protein andbone turnover; increase responsiveness tocatecholamines; necessary for fetal and infantgrowth and development
Major Actions and Source of HormonesTHYROID C CELLS1. Calcitonin• Lowers blood calcium and phosphate levels
Role of Iodine• essential to the thyroid gland for synthesis of itshormones• thyroid gland is extremely efficient in taking upiodide from the blood and concentrating it withinthe cells, where iodide ions are converted toiodine molecules, which react with tyrosine (anamino acid) to form the thyroid hormones
Regulation of Thyroid HormoneHYPOTHALAMIC-PITUITARY-THYROID AXIS
Thyroid Function Tests• laboratory measurement of thyroid hormones serum immunoassay for TSH and freethyroxine (FT4)• thyroid scanning• biopsy• ultrasonography
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearsthereafterThyroid Stimulating Hormone• Measurement of the serum TSH concentrationis the single best screening test of thyroidfunction because of its high sensitivity.• Values above the normal range of 0.4 to 6.15μU/mL indicate primary hypothyroidism, andlow values indicate hyperthyroidism.Current recommendations suggest TSH screeningfor all adults beginning at age 35, and every 5 yearsthereafter.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearsthereafterSerum Free Thyroxine• The test most commonly used to confirm anabnormal TSH is FT4.• FT4 is a direct measurement of free (unbound)thyroxine, the only metabolically active fractionof T4. The range of FT4 in serum is normally0.9 to 1.7 ng/dL (11.5 to 21.8 pmol/L).
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearsthreafterSerum T3 and T4• Measurement of total T3 or T4 includesprotein-bound and free hormone levels thatoccur in response to TSH secretion.• Normal range for T4 is 4.5 to 11.5 μg/dL (58.5to 150 nmol/L).• The normal range for serum T3 is 70 to 220μg/dL (1.15 to 3.10 nmol/L).
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearsthreafterT3 Resin Uptake Test• The T3 resin uptake test is an indirect measureof unsaturated TBG.• Its purpose is to determine the amount ofthyroid hormone bound to TBG and thenumber of available binding sites.• The normal T3 uptake value is 25% to 35%(relative uptake fraction, 0.25 to 0.35), whichindicates that about one third of the availablesites of TBG are occupied by thyroid hormone.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearsthreafterThyroid Antibodies• Antithyroid antibody titers are normally present in5% to 10% of the population and increase withage.Radioactive Iodine Uptake• The radioactive iodine uptake test measures therate of iodine uptake by the thyroid gland.• It measures the proportion of the administereddose present in the thyroid gland at a specific timeafter its administration.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearsthreafterFine Needle Aspiration Biopsy• It is often the initial test for evaluation of thyroidmasses.• Results are reported as:1. negative (benign)2. positive (malignant)3. indeterminate (suspicious)4. inadequate (nondiagnostic)
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearsthreafterThyroid Scan, Radioscan, and Scintiscan• In a thyroid scan, a scintillation detector or gammacamera moves back and forth across the area to bestudied in a series of parallel tracks, and a visualimage is made of the distribution of radioactivity inthe area being scanned.• Scans are helpful in determining the location, size,shape, and anatomic function of the thyroid gland,particularly when thyroid tissue is substernal orlarge.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterOther Diagnostic Tests• Ultrasound, CT scans, and MRI may be used toclarify or confirm the results of other diagnosticstudies.• Thyroglobulin (Tg), a precursor for T3 and T4,can be measured reliably in the serum byradioimmunoassay.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterNursing Implications• When thyroid tests are scheduled, it is necessary todetermine whether the patient has takenmedications or agents that contain iodine becausethese may alter the test results.• Sources of iodine are topical antiseptics,multivitamin preparations, and food supplementsfrequently found in health food stores; cough syrups;and amiodarone, an antiarrhythmic agent.• Other medications that may affect test results areestrogens, salicylates, amphetamines,chemotherapeutic agents, antibiotics,corticosteroids, and mercurial diuretics.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterAbnormal Thyroid Function• Inadequate secretion of thyroid hormone duringfetal and neonatal development results in stuntedphysical and mental growth because of generaldepression of metabolic activity.• In adults, hypothyroidism manifests as lethargy,slow mentation, and generalized slowing of bodyfunctions.Myxedema is the worst-case scenario ofhypothyroidism. If a test question says“myxedema,” think hypothyroidism.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterHypothyroidism• Hypothyroidism results from suboptimal levels of thyroidhormone.• Thyroid deficiency can affect all body functions and canrange from mild, subclinical forms to myxedema, anadvanced form.• The most common cause of hypothyroidism in adults isautoimmune thyroiditis (Hashimoto’s disease), in whichthe immune system attacks the thyroid gland.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterClinical Manifestations• Early symptoms of hypothyroidism are nonspecific, butextreme fatigue makes it difficult for the person tocomplete a full day’s work or participate in usualactivities.• Reports of hair loss, brittle nails, and dry skin arecommon, and numbness and tingling of the fingers mayoccur.• On occasion, the voice may become husky, and thepatient may complain of hoarseness.• Menstrual disturbances such as menorrhagia oramenorrhea occur, in addition to loss of libido.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterClinical Manifestations• Hypothyroidism affects women five times morefrequently than men and occurs most often between 30and 60 years of age.• Severe hypothyroidism results in a subnormaltemperature and pulse rate.• The patient usually begins to gain weight even withoutan increase in food intake, although severelyhypothyroid patients may be cachectic.• The skin becomes thickened because of anaccumulation accumulation of mucopolysaccharides inthe subcutaneous tissues.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterClinical Manifestations• The hair thins and falls out; the face becomesexpressionless and masklike.• The patient often complains of being cold even in awarm environment.• At first, the patient may be irritable and may complain offatigue, but as the condition progresses, the emotionalresponses are subdued.• The mental processes become dulled, and the patientappears apathetic.• Speech is slow, the tongue enlarges, and hands andfeet increase in size.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterClinical Manifestations• The patient frequently complains of constipation.• Deafness may also occur.• Advanced hypothyroidism may produce personality andcognitive changes characteristic of dementia.• Inadequate ventilation and sleep apnea can occur withsevere hypothyroidism.• Pleural effusion, pericardial effusion, and respiratorymuscle weakness may also occur.• Severe hypothyroidism is associated with an elevatedserum cholesterol level, atherosclerosis, coronary arterydisease, and poor left ventricular function.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterClinical Manifestations• The patient with advanced hypothyroidism ishypothermic and abnormally sensitive to sedatives,opioids, and anesthetic agents.• Patients with unrecognized hypothyroidism who areundergoing surgery are at increased risk forintraoperative hypotension and postoperative heartfailure and altered mental status.• Myxedema coma describes the most extreme, severestage of hypothyroidism, in which the patient ishypothermic and unconscious.• Myxedema coma may follow increasing lethargy,progressing to stupor and then coma.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterClinical Manifestations• The patient’s respiratory drive is depressed, resulting inalveolar hypoventilation, progressive CO2 retention,narcosis, and coma.• These symptoms, along with cardiovascular collapseand shock, require aggressive and intensive therapy ifthe patient is to survive.• Even with early vigorous therapy, however, mortality ishigh.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterMedical ManagementPHARMACOLOGIC THERAPY• Synthetic levothyroxine (Synthroid or Levothroid) is thepreferred preparation for treating hypothyroidism andsuppressing nontoxic goiters.• Desiccated thyroid is used less frequently because itoften results in transient elevated serum concentrationsof T3, with occasional symptoms of hyperthyroidism.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterMedical ManagementPREVENTION OF CARDIAC DYSFUNCTION• Any patient who has had hypothyroidism for a longperiod is almost certain to have elevated serumcholesterol levels, atherosclerosis, and coronary arterydisease.• The occurrence of angina is the signal that the oxygenneeds of the myocardium exceed its blood supply.• Angina or dysrhythmias may occur when thyroidreplacement is initiated because thyroid hormonesenhance the cardiovascular effects of catecholamines.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterMedical ManagementPREVENTION OF CARDIAC DYSFUNCTION• Angina or dysrhythmias may occur when thyroidreplacement is initiated because thyroid hormonesenhance the cardiovascular effects of catecholamines.• If angina or dysrhythmias occur, thyroid hormoneadministration must be discontinued immediately.• Later, when it can be resumed safely, thyroid hormonereplacement should be prescribed cautiously at a lowerdosage and under the close observation of the physicianand the nurse.
Current recommendations suggestTSH screening for all adults beginning at age 35, and every 5 yearshreafterMedical ManagementPREVENTION OF MEDICATION INTERACTIONS• Thyroid hormones may increase blood glucose levels,which may necessitate adjustment in the dosage of insulinor oral antidiabetic agents in patients with diabetes.• The effects of thyroid hormone may be increased byphenytoin (Dilantin) and tricyclic antidepressant agents.• Thyroid hormones may also increase the pharmacologiceffects of digitalis glycosides, anticoagulant agents, andindomethacin, requiring careful observation andassessment by the nurse for side effects.• Bone loss and osteoporosis may also occur with thyroidtherapy.
SUPPORTIVE THERAPYIn severe hypothyroidism and myxedema coma, managementincludes maintaining vital functions. Arterial blood gases may bemeasured to determine CO2 retention and to guide the use ofassisted ventilation to combat hypoventilation. Pulse oximetrymay also be helpful in monitoring oxygen saturation levels. Fluidsare administered cautiously because of the danger of water intoxication.Application of external heat (eg, heating pads) is avoidedbecause it increases oxygen requirements and may lead to vascularcollapse. If hypoglycemia is evident, concentrated glucosemay be prescribed to provide glucose without precipitating fluidoverload. Thyroid hormone (usually Synthroid) is administeredintravenously until consciousness is restored if myxedema hasprogressed to myxedema coma. The patient is then continued onoral thyroid hormone therapy. Because of an associated adrenocorticalinsufficiency, corticosteroid therapy may be necessary.Medical ManagementSUPPORTIVE THERAPY• In severe hypothyroidism and myxedema coma,management includes maintaining vital functions.• Arterial blood gases may be measured to determine CO2retention and to guide the use of assisted ventilation tocombat hypoventilation.• Pulse oximetry may also be helpful in monitoring oxygensaturation levels.• Fluids are administered cautiously because of the dangerof water intoxication.• Application of external heat is avoided because it increasesoxygen requirements and may lead to vascular collapse.
SUPPORTIVE THERAPYIn severe hypothyroidism and myxedema coma, managementincludes maintaining vital functions. Arterial blood gases may bemeasured to determine CO2 retention and to guide the use ofassisted ventilation to combat hypoventilation. Pulse oximetrymay also be helpful in monitoring oxygen saturation levels. Fluidsare administered cautiously because of the danger of water intoxication.Application of external heat (eg, heating pads) is avoidedbecause it increases oxygen requirements and may lead to vascularcollapse. If hypoglycemia is evident, concentrated glucosemay be prescribed to provide glucose without precipitating fluidoverload. Thyroid hormone (usually Synthroid) is administeredintravenously until consciousness is restored if myxedema hasprogressed to myxedema coma. The patient is then continued onoral thyroid hormone therapy. Because of an associated adrenocorticalinsufficiency, corticosteroid therapy may be necessary.Medical ManagementSUPPORTIVE THERAPY• If hypoglycemia is evident, concentrated glucose may beprescribed to provide glucose without precipitating fluidoverload.• Thyroid hormone (usually Synthroid) is administeredintravenously until consciousness is restored ifmyxedema has progressed to myxedema coma.• The patient is then continued on oral thyroid hormonetherapy.• Because of an associated adrenocortical insufficiency,corticosteroid therapy may be necessary.
SUPPORTIVE THERAPYIn severe hypothyroidism and myxedema coma, managementincludes maintaining vital functions. Arterial blood gases may bemeasured to determine CO2 retention and to guide the use ofassisted ventilation to combat hypoventilation. Pulse oximetrymay also be helpful in monitoring oxygen saturation levels. Fluidsare administered cautiously because of the danger of water intoxication.Application of external heat (eg, heating pads) is avoidedbecause it increases oxygen requirements and may lead to vascularcollapse. If hypoglycemia is evident, concentrated glucosemay be prescribed to provide glucose without precipitating fluidoverload. Thyroid hormone (usually Synthroid) is administeredintravenously until consciousness is restored if myxedema hasprogressed to myxedema coma. The patient is then continued onoral thyroid hormone therapy. Because of an associated adrenocorticalinsufficiency, corticosteroid therapy may be necessary.Nursing ManagementMODIFYING ACTIVITY• The patient with hypothyroidism experiences decreasedenergy and moderate to severe lethargy. As a result, therisk for complications from immobility increases.• The patient’s ability to exercise and participate inactivities is further limited by the changes incardiovascular and pulmonary status secondary tohypothyroidism.• A major role of the nurse is assisting with care andhygiene while encouraging the patient to participate inactivities within established tolerance levels to preventthe complications of immobility.
SUPPORTIVE THERAPYIn severe hypothyroidism and myxedema coma, managementincludes maintaining vital functions. Arterial blood gases may bemeasured to determine CO2 retention and to guide the use ofassisted ventilation to combat hypoventilation. Pulse oximetrymay also be helpful in monitoring oxygen saturation levels. Fluidsare administered cautiously because of the danger of water intoxication.Application of external heat (eg, heating pads) is avoidedbecause it increases oxygen requirements and may lead to vascularcollapse. If hypoglycemia is evident, concentrated glucosemay be prescribed to provide glucose without precipitating fluidoverload. Thyroid hormone (usually Synthroid) is administeredintravenously until consciousness is restored if myxedema hasprogressed to myxedema coma. The patient is then continued onoral thyroid hormone therapy. Because of an associated adrenocorticalinsufficiency, corticosteroid therapy may be necessary.Nursing ManagementMONITORING PHYSICAL STATUS• The nurse closely monitors the patient’s vital signs andcognitive level to detect the following: Deterioration of physical and mental status Signs and symptoms indicating that treatment hasresulted in the metabolic rate exceeding the ability ofthe cardiovascular and pulmonary systems to respond Continued limitations or complications of myxedema
SUPPORTIVE THERAPYIn severe hypothyroidism and myxedema coma, managementincludes maintaining vital functions. Arterial blood gases may bemeasured to determine CO2 retention and to guide the use ofassisted ventilation to combat hypoventilation. Pulse oximetrymay also be helpful in monitoring oxygen saturation levels. Fluidsare administered cautiously because of the danger of water intoxication.Application of external heat (eg, heating pads) is avoidedbecause it increases oxygen requirements and may lead to vascularcollapse. If hypoglycemia is evident, concentrated glucosemay be prescribed to provide glucose without precipitating fluidoverload. Thyroid hormone (usually Synthroid) is administeredintravenously until consciousness is restored if myxedema hasprogressed to myxedema coma. The patient is then continued onoral thyroid hormone therapy. Because of an associated adrenocorticalinsufficiency, corticosteroid therapy may be necessary.Nursing ManagementPROMOTING PHYSICAL COMFORT• The patient often experiences chilling and extremeintolerance to cold, even if the room feels comfortable orhot to others.• Extra clothing and blankets are provided, and the patientis protected from drafts.• Use of heating pads and electric blankets is avoidedbecause of the risk of peripheral vasodilation, furtherloss of body heat, and vascular collapse.• Additionally, the patient could be burned by these itemswithout being aware of it because of delayed responsesand decreased mental status.
SUPPORTIVE THERAPYInNursing ManagementPROVIDING EMOTIONAL SUPPORT• The patient with moderate to severe hypothyroidism mayexperience severe emotional reactions to changes inappearance and body image and the frequent delay indiagnosis.• As hypothyroidism is treated successfully and symptomssubside, the patient may experience depression andguilt as a result of the progression and severity ofsymptoms that occurred.• The nurse informs the patient and family that thesymptoms and inability to recognize them are commonand part of the disorder itself.
SUPPORTIVE THERAPYInNursing ManagementPROVIDING EMOTIONAL SUPPORT• The patient and family may require assistance andcounseling to deal with the emotional concerns andreactions that result.
SUPPORTIVE THERAPYInHyperthyroidism• Graves’ disease, results from an excessive output ofthyroid hormones caused by abnormal stimulation of thethyroid gland by circulating immunoglobulins.• It may appear after an emotional shock, stress, or aninfection, but the exact significance of these relationships isnot understood.• Other common causes of hyperthyroidism includethyroiditis and excessive ingestion of thyroid hormone.Hyperthyroidism is mainly seen in females and ismost common after childbirth or duringmenopause.
SUPPORTIVE THERAPYInClinical Manifestations• Patients with well-developed hyperthyroidism exhibit acharacteristic group of signs and symptoms(thyrotoxicosis).• The presenting symptom is often nervousness.• These patients are often emotionally hyperexcitable,irritable, and apprehensive; they cannot sit quietly; theysuffer from palpitations; and their pulse is abnormallyrapid at rest as well as on exertion.• They tolerate heat poorly and perspire unusually freely.• The skin is flushed continuously, with a characteristicsalmon color, and is likely to be warm, soft, and moist.
SUPPORTIVE THERAPYInClinical Manifestations• Elderly patients, however, may report dry skin and diffusepruritus. A fine tremor of the hands may be observed.• Patients may exhibit exophthalmos, which produces astartled facial expression.• Other manifestations include an increased appetite anddietary intake, progressive weight loss, abnormal muscularfatigability and weakness, amenorrhea, and changes inbowel function.• The pulse rate ranges constantly between 90 and 160beats/min; the systolic, but characteristically not thediastolic, blood pressure is elevated; atrial fibrillation mayoccur; and cardiac decompensation in the form of heartfailure is common, especially in elderly patients.
SUPPORTIVE THERAPYInClinical Manifestations• Osteoporosis and fracture are also associated withhyperthyroidism.• Cardiac effects may include sinus tachycardia ordysrhythmias, increased pulse pressure, andpalpitations; it has been suggested that these changesmay be related to increased sensitivity tocatecholamines or to changes in neurotransmitterturnover.• Myocardial hypertrophy and heart failure may occur ifthe hyperthyroidism is severe and untreated.• The course of the disease may be mild, characterized byremissions and exacerbations and terminating withspontaneous recovery in a few months or years.
SUPPORTIVE THERAPYInClinical Manifestations• Conversely, it may progress relentlessly, with theuntreated person becoming emaciated, intenselynervous, delirious, and even disoriented; eventually, theheart fails.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• The thyroid gland invariably is enlarged to some extent.• It is soft and may pulsate; a thrill often can be palpated,and a bruit is heard over the thyroid arteries.• In advanced cases, the diagnosis is made on the basisof the symptoms and an increase in serum T4 and anincreased 123I or 125I uptake by the thyroid in excess of50%.
SUPPORTIVE THERAPYInThyroid Storm• Thyroid storm (thyrotoxic crisis) is a form of severehyperthyroidism, usually of abrupt onset.• Untreated it is almost always fatal, but with propertreatment the mortality rate is reduced substantially.• The patient with thyroid storm or crisis is critically ill andrequires astute observation and aggressive andsupportive nursing care during and after the acute stageof illness.
SUPPORTIVE THERAPYInThyroid StormThyroid storm is characterized by:• High fever (hyperpyrexia) above 38.5°C• Extreme tachycardia (more than 130 beats/min)• Exaggerated symptoms of hyperthyroidism withdisturbances of a major system—for example, GI(weight loss, diarrhea, abdominal pain), orcardiovascular (edema, chest pain, dyspnea,palpitations)• Altered neurologic or mental state, which frequentlyappears as delirium psychosis, somnolence, or coma
SUPPORTIVE THERAPYInThyroid Storm• Life-threatening thyroid storm is usually precipitated bystress, such as injury, infection, thyroid and nonthyroidsurgery, tooth extraction, insulin reaction, diabeticacidosis, pregnancy, digitalis intoxication, abruptwithdrawal of antithyroid medications, extremeemotional stress, or vigorous palpation of the thyroid.• These factors can precipitate thyroid storm in thepartially controlled or completely untreated patient withhyperthyroidism.
SUPPORTIVE THERAPYInThyroid StormMANAGEMENT• Immediate objectives are reduction of body temperatureand heart rate and prevention of vascular collapse.Measures to accomplish these objectives include:• A hypothermia mattress or blanket, ice packs, a coolenvironment, hydrocortisone, and acetaminophen(Tylenol).• Salicylates (eg, aspirin) are not used because theydisplace thyroid hormone from binding proteins andworsen the hypermetabolism.• Humidified oxygen is administered to improve tissueoxygenation and meet the high metabolic demands.
SUPPORTIVE THERAPYInThyroid StormMANAGEMENT• Arterial blood gas levels or pulse oximetry may be used tomonitor respiratory status.• Intravenous fluids containing dextrose are administered toreplace liver glycogen stores that have been decreased inthe hyperthyroid patient.• PTU or methimazole is administered to impede formationof thyroid hormone and block conversion of T4 to T3, themore active form of thyroid hormone.• Hydrocortisone is prescribed to treat shock or adrenalinsufficiency.• Iodine is administered to decrease output of T4 from thethyroid gland.
SUPPORTIVE THERAPYInThyroid StormMANAGEMENT• For cardiac problems such as atrial fibrillation,dysrhythmias, and heart failure, sympatholytic agentsmay be administered.• Propranolol, combined with digitalis, has been effectivein reducing severe cardiac symptoms.
SUPPORTIVE THERAPYInMedical Management• Treatment of hyperthyroidism is directed toward reducingthyroid hyperactivity to relieve symptoms and remove thecause of important complications.PHARMACOLOGIC THERAPY• Two forms of pharmacotherapy are available for treatinghyperthyroidism and controlling excessive thyroid activity:1. use of irradiation by administration of the radioisotope123I or 131I for destructive effects on the thyroid glandand2. antithyroid medications that interfere with the synthesisof thyroid hormones and other agents that controlmanifestations of hyperthyroidism.
SUPPORTIVE THERAPYInMedical ManagementRADIOACTIVE IODINE THERAPY• The goal of radioactive iodine therapy (123I or 131I) is todestroy the overactive thyroid cells.• The patient is instructed about what to expect with thistasteless, colorless radioiodine, which may beadministered by the radiologist.• About 70% to 85% of patients are cured by one dose ofradioactive iodine.• The patient is observed for signs of thyroid storm;propranolol is useful in controlling these symptoms.
SUPPORTIVE THERAPYInMedical ManagementRADIOACTIVE IODINE THERAPY• Radioactive iodine has been used to treat toxicadenomas and multinodular goiter and most varieties ofthyrotoxicosis; it is preferred for treating patients beyondthe childbearing years with diffuse toxic goiter.• It is contraindicated in pregnancy and in nursing mothersbecause radioiodine crosses the placenta and issecreted in breast milk.• A major advantage of treatment with radioactive iodine isthat it avoids many of the side effects associated withantithyroid medications.
SUPPORTIVE THERAPYInMedical ManagementANTITHYROID MEDICATIONS• Antithyroid agents block the utilization of iodine byinterfering with the iodination of thyrosine and thecoupling of iodothyrosines in the synthesis of thyroidhormones.• The most commonly used medications arepropylthiouracil (Propacil, PTU) or methimazole(Tapazole) until the patient is euthyroid (ie, neitherhyperthyroid nor hypothyroid).Agranulocytosis can develop as a side effect of theantithyroid drugs. Signs of this include sore mouth, sorethroat, rash, and fever. A white blood cell count should bechecked prior to initiating therapy.
SUPPORTIVE THERAPYInMedical ManagementANTITHYROID MEDICATIONS• Toxic complications of antithyroid medications arerelatively uncommon; nevertheless, the importance ofperiodic follow-up is emphasized because medicationsensitization, fever, rash, urticaria, or evenagranulocytosis and thrombocytopenia may develop.• With any sign of infection, especially pharyngitis andfever or the occurrence of mouth ulcers, the patient isadvised to stop the medication, notify the physicianimmediately, and undergo hematologic studies.
SUPPORTIVE THERAPYInMedical ManagementANTITHYROID MEDICATIONS• Patients taking antithyroid medications are instructed not touse decongestants for nasal stuffiness because they arepoorly tolerated.• Antithyroid medications are contraindicated in latepregnancy because they may produce goiter and cretinismin the fetus.• Thyroid hormone is available as thyroglobulin (Proloid) andlevothyroxine sodium (Synthroid). These slow-actingpreparations take about 10 days to achieve their full effect.• Liothyronine sodium (Cytomel) has a more rapid onset, andits action is of short duration.
SUPPORTIVE THERAPYInMedical ManagementADJUNCTIVE THERAPY• Iodine or iodide compounds, decrease the release ofthyroid hormones from the thyroid gland and reduce thevascularity and size of the thyroid.• Compounds such as potassium iodide (KI), Lugol’ssolution, and saturated solution of potassium iodide(SSKI) may be used in combination with antithyroidagents or beta-adrenergic blockers to prepare thepatient with hyperthyroidism for surgery.There are two types of iodine: dietary iodine andmedicinal iodine. They each have totally differentactions.
SUPPORTIVE THERAPYInMedical ManagementADJUNCTIVE THERAPY• These agents reduce the activity of the thyroid hormoneand the vascularity of the thyroid gland, making thesurgical procedure safer.• Solutions of iodine and iodide compounds are morepalatable in milk or fruit juice and are administered througha straw to prevent staining of the teeth.• Beta-adrenergic blocking agents are important incontrolling the sympathetic nervous system effects ofhyperthyroidism.Asthmatics and diabetics should not be given beta-blockers. Beta-blockers can cause bronchospasmand mask the signs of hypoglycemia.
SUPPORTIVE THERAPYInMedical ManagementSURGICAL MANAGEMENT• Surgery is reserved in pregnant women allergic toantithyroid medications, patients with large goiters, orpatients unable to take antithyroid agents.• The surgical removal of about five sixths of the thyroidtissue (subtotal thyroidectomy) practically ensures aprolonged remission in most patients with exophthalmicgoiter.Be sure to watch for hypocalcemia postopthyroidectomy, as this electrolyte imbalance canaffect the airway, the heart, and cause seizures!
SUPPORTIVE THERAPYInMedical ManagementSURGICAL MANAGEMENT• Its use is reserved for large goiters, presence ofobstructive symptoms, pregnant women, or when thereis a need for rapid normalization of thyroid function.• Before surgery, propylthiouracil is administered untilsigns of hyperthyroidism have disappeared.• A beta-adrenergic blocking agent (propranolol) may beused to reduce the heart rate and other signs andsymptoms of hyperthyroidism; however, this does notcreate a euthyroid state.
SUPPORTIVE THERAPYInMedical ManagementSURGICAL MANAGEMENT• Iodine (Lugol’s solution or potassium iodide) may beprescribed in an effort to reduce blood loss; however, theeffectiveness of this is unknown.• Patients receiving iodine medication must be monitoredfor evidence of iodine toxicity (iodism), which requiresimmediate withdrawal of the medication.• Symptoms of iodism include swelling of the buccalmucosa, excessive salivation, coryza, and skineruptions.
SUPPORTIVE THERAPYInRecurrent Hyperthyroidism• No treatment for thyrotoxicosis is without side effects,and all three treatments (radioactive iodine therapy,antithyroid medications, and surgery) share the samecomplications: relapse or recurrent hyperthyroidism andpermanent hypothyroidism.• The relapse rate after radioactive iodine therapydepends on the dose used in treatment.Post radioactive iodine. The client should stay awayfrom babies, not kiss anyone, and cover the mouthand nose when coughing and sneezing for 24 hoursafter treatment as the iodine can be shed in saliva.
SUPPORTIVE THERAPYInRecurrent Hyperthyroidism• Hypothyroidism occurs in almost 80% of patients at 1year and in 90% to 100% by 5 years for both the multiple• low-dose and single high-dose methods.• Although rates of relapse and the occurrence ofhypothyroidism vary, relapse with antithyroidmedications is about 45% by 1 year after completion oftherapy and almost 75% by 5 years later.• Discontinuation of antithyroid medications beforetherapy is complete usually results in relapse within 6months in most patients.
SUPPORTIVE THERAPYInThyroiditis• Thyroiditis, inflammation of the thyroid gland, can beacute, subacute, or chronic. Each type of thyroiditis ischaracterized by inflammation, fibrosis, or lymphocyticinfiltration of the thyroid gland.ACUTE THYROIDITIS• Acute thyroiditis is a rare disorder caused by infection ofthe thyroid gland by bacteria, fungi, mycobacteria, orparasites.• Staphylococcus aureus and other staphylococci are themost common causes.• Infection typically causes anterior neck pain andswelling, fever, dysphagia, and dysphonia.
SUPPORTIVE THERAPYInThyroiditis• Pharyngitis or pharyngeal pain is often present.• Examination may reveal warmth, erythema, andtenderness of the thyroid gland.• Treatment of acute thyroiditis in includes antimicrobialagents and fluid replacement.• Surgical incision and drainage may be needed if anabscess is present.
SUPPORTIVE THERAPYInThyroiditisSUBACUTE THYROIDITIS• Subacute thyroiditis may be subacute granulomatousthyroiditis (deQuervain’s thyroiditis) or painlessthyroiditis (silent thyroiditis or subacute lymphocyticthyroiditis).• Subacute granulomatous thyroiditis is an inflammatorydisorder of the thyroid gland that predominantly affectswomen between 40 and 50 years old.• The condition presents as a painful swelling in theanterior neck that lasts 1 to 2 months and thendisappears spontaneously without residual effect.
SUPPORTIVE THERAPYInThyroiditisSUBACUTE THYROIDITIS• The thyroid enlarges symmetrically and may be painful.• The overlying skin is often reddened and warm.• Swallowing may be difficult and uncomfortable.• Irritability, nervousness, insomnia, and weight loss—manifestations of hyperthyroidism—are common, andmany patients experience chills and fever as well.• Treatment aims to control the inflammation, nonsteroidalanti-inflammatory drugs (NSAIDs) are used to relieveneck pain.
SUPPORTIVE THERAPYInThyroiditisSUBACUTE THYROIDITIS• Acetylsalicylic acid is avoided if symptoms ofhyperthyroidism occur because aspirin displaces thyroidhormone from its binding sites and increases theamount of circulating hormone.• Beta-blocking agents (eg, propranolol [Inderal]) may beused to control symptoms of hyperthyroidism.• Antithyroid agents, which block the synthesis of T3 andT4, are not effective in thyroiditis because theassociated thyrotoxicosis results from the release ofstored thyroid hormones rather than from their increasedsynthesis.
SUPPORTIVE THERAPYInThyroiditisSUBACUTE THYROIDITIS• In more severe cases, oral corticosteroids may beprescribed to reduce swelling and relieve pain; however,they do not usually affect the underlying cause.• In some cases, temporary hypothyroidism may developand may necessitate thyroid hormone therapy.• Follow-up monitoring is necessary to document thepatient’s return to a euthyroid state.• Painless thyroiditis (subacute lymphocytic thyroiditis)often occurs in the postpartum period and is thought tobe an autoimmune process.
SUPPORTIVE THERAPYInThyroiditisSUBACUTE THYROIDITIS• Treatment is directed at symptoms, and yearly follow-upis recommended to determine the patient’s need fortreatment of subsequent hypothyroidism.
SUPPORTIVE THERAPYInThyroiditisCHRONIC THYROIDITIS (HASHIMOTO’S DISEASE)• Chronic thyroiditis, which occurs most frequently in womenbetween 30 and 50 years old, has been termedHashimoto’s disease, or chronic lymphocytic thyroiditis; itsdiagnosis is based on the histologic appearance of theinflamed gland.• In contrast to acute thyroiditis, the chronic forms areusually not accompanied by pain, pressure symptoms, orfever, and thyroid activity is usually normal or low ratherthan increased.• Cell-mediated immunity may play a significant role in thepathogenesis of chronic thyroiditis, and there may be agenetic predisposition to it.
SUPPORTIVE THERAPYInThyroiditisCHRONIC THYROIDITIS (HASHIMOTO’S DISEASE)• If untreated, the disease runs a slow, progressivecourse, leading eventually to hypothyroidism.• The objective of treatment is to reduce the size of thethyroid gland and prevent hypothyroidism.• Thyroid hormone therapy is prescribed to reduce thyroidactivity and the production of thyroglobulin.Hashimoto’s thyroiditis can cause hyperthyroidismor hypothyroidism. The client’s symptoms dependon which phase of the disease she is in.
SUPPORTIVE THERAPYInThyroid Tumor• Tumors of the thyroid gland are classified on the basis ofbeing benign or malignant, the presence or absence ofassociated thyrotoxicosis, and the diffuse or irregularquality of the glandular enlargement.• If the enlargement is sufficient to cause a visible swellingin the neck, the tumor is referred to as a goiter.• All grades of goiter are encountered, from those that arebarely visible to those producing disfigurement.• Some are symmetric and diffuse; others are nodular.Some are accompanied by hyperthyroidism, in whichcase they are described as toxic; others are associatedwith a euthyroid state and are called nontoxic goiters.
SUPPORTIVE THERAPYInEndemic Goiter• The most common type of goiter, encountered chiefly ingeographic regions where the natural supply of iodine isdeficient, is the so-called simple or colloid goiter.• In addition to being caused by an iodine deficiency,simple goiter may be caused by an intake of largequantities of goitrogenic substances in patients withunusually susceptible glands.• These substances include excessive amounts of iodineor lithium, which is used in treating bipolar disorders.Excessive palpation of a goiter can cause a releaseof thyroid hormone that could throw the client intothyroid storm.
SUPPORTIVE THERAPYInEndemic Goiter• The pituitary gland produces thyrotropin or TSH, ahormone that controls the release of thyroid hormonefrom the thyroid gland.• Its production increases if there is subnormal thyroidactivity, as when insufficient iodine is available forproduction of the thyroid hormone.• Such goiters usually cause no symptoms, except for theswelling in the neck, which may result in trachealcompression when excessive.• Many goiters of this type recede after iodine imbalanceis corrected.
SUPPORTIVE THERAPYInEndemic Goiter• Supplementary iodine, such as SSKI, is prescribed tosuppress the pituitary’s thyroid-stimulating activity.• When surgery is recommended, the risk forpostoperative complications is minimized by ensuring apreoperative euthyroid state by treatment withantithyroid medications and iodide to reduce the sizeand vascularity of the goiter.• Providing children in iodine-poor regions with iodinecompounds can prevent simple or endemic goiter. If themean iodine intake is less than 40 fg/day, the thyroidgland hypertrophies.
SUPPORTIVE THERAPYInNodular Goiter• Some thyroid glands are nodular because of areas ofhyperplasia.• No symptoms may arise as a result of this condition, butnot uncommonly these nodules slowly increase in size,with some descending into the thorax, where they causelocal pressure symptoms.• Some nodules become malignant, and some areassociated with a hyperthyroid state.• Thus, the patient with many thyroid nodules mayeventually require surgery.
SUPPORTIVE THERAPYInThyroid Cancer• Cancer of the thyroid is much less prevalent than otherforms of cancer; however, it accounts for 90% ofendocrine malignancies.• There are several types of cancer of the thyroid gland;the type determines the course and prognosis.• External radiation of the head, neck, or chest in infancyand childhood increases the risk of thyroid carcinoma.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• Lesions that are single, hard, and fixed on palpation orassociated with cervical lymphadenopathy suggestmalignancy.• Thyroid function tests may be helpful in evaluatingthyroid nodules and masses; however, their results arerarely conclusive.• Needle biopsy of the thyroid gland is used as anoutpatient procedure to make a diagnosis of thyroidcancer, to differentiate cancerous thyroid nodules fromnoncancerous nodules, and to stage the cancer ifdetected.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• A second type of aspiration or biopsy uses a largeboreneedle rather than the fine needle used in standardbiopsy; it may be used when the results of the standardbiopsy are inconclusive, or with rapidly growing tumors.• Additional diagnostic studies include ultrasound, MRI,CT scans, thyroid scans, radioactive iodine uptakestudies, and thyroid suppression tests.
SUPPORTIVE THERAPYInMedical Management• The treatment of choice for thyroid carcinoma is surgicalremoval.• Total or near-total thyroidectomy is performed whenpossible.• Modified neck dissection or more extensive radical neckdissection is performed if there is lymph nodeinvolvement.• Efforts are made to spare parathyroid tissue to reducethe risk for postoperative hypocalcemia and tetany.• After surgery, ablation procedures are carried out withradioactive iodine to eradicate residual thyroid tissue ifthe tumor is radiosensitive.
SUPPORTIVE THERAPYInMedical Management• Radioactive iodine also maximizes the chance ofdiscovering thyroid metastasis at a later date if total-bodyscans are carried out.• After surgery, thyroid hormone is administered insuppressive doses to lower the levels of TSH to a euthyroidstate.• If remaining thyroid tissue is inadequate to producesufficient thyroid hormone, thyroxine is requiredpermanently.• The patient who receives external sources of radiationtherapy is at risk for mucositis, dryness of the mouth,dysphagia, redness of the skin, anorexia, and fatigue.• Chemotherapy is infrequently used to treat thyroid cancer.
SUPPORTIVE THERAPYInMedical Management• Postoperatively, the patient is instructed to takeexogenous thyroid hormone to prevent hypothyroidism.• Later follow-up includes clinical assessment forrecurrence of nodules or masses in the neck and signsof hoarseness, dysphagia, or dyspnea.• Total body scans are performed 2 to 4 months aftersurgery to detect residual thyroid tissue or metastaticdisease.• FT4, TSH, serum calcium, and phosphorus levels aremonitored to determine whether the thyroid hormonesupplementation is adequate and to note whethercalcium balance is maintained.
SUPPORTIVE THERAPYInMedical Management• Although local and systemic reactions to radiation mayoccur and may include neutropenia orthrombocytopenia, these complications are rare whenradioactive iodine is used.• Patients who undergo surgery that is combined withradioiodine have a higher survival rate than thoseundergoing surgery alone.• Patient teaching emphasizes the importance of takingprescribed medications and following recommendationsfor follow-up monitoring.
SUPPORTIVE THERAPYInNursing Management• Important preoperative goals are to gain the patient’sconfidence and reduce anxiety.• Often, the patient’s home life has become tensebecause of his or her restlessness, irritability, andnervousness secondary to hyperthyroidism.• Efforts are necessary to protect the patient from suchtension and stress to avoid precipitating thyroid storm.• If the patient reports increased stress when with familyor friends, suggestions are made to limit contact withthem.• Quiet and relaxing forms of recreation or occupationaltherapy may be helpful.
SUPPORTIVE THERAPYInParathyroid Disorders• Parathormone, the protein hormone from the parathyroidglands, regulates calcium and phosphorus metabolism.• Increased secretion of parathormone results inincreased calcium absorption from the kidney, intestine,and bones, thereby raising the blood calcium level.• Some actions of this hormone are increased by thepresence of vitamin D.• Parathormone also tends to lower the blood phosphoruslevel.PTH makes the serum calcium increase.
Major Actions and Source of HormonesPARATHYROID GLANDS1. Parathyroid hormone• Regulates serum calciumRemember, calcium and phosphorus have aninverse relationship. When one is elevated, theother is decreased.
SUPPORTIVE THERAPYInParathyroid Disorders• When the product of serum calcium and serumphosphorus (calcium × phosphorus) rises, calciumphosphate may precipitate in various organs of the bodyand cause tissue calcification.• The serum level of ionized calcium regulates the outputof parathormone.• Increased serum calcium results in decreasedparathormone secretion, creating a negative feedbacksystem.
SUPPORTIVE THERAPYInHyperparathyroidism• Hyperparathyroidism, which is caused by overproductionof parathyroid hormone by the parathyroid glands, ischaracterized by bone decalcification and thedevelopment of renal calculi containing calcium.• Primary hyperparathyroidism occurs two to four timesmore often in women than in men and is most commonin patients between 60 and 70 years of age.• The disease is rare in children younger than 15 years,but the incidence increases tenfold between the ages of15 and 65 years.• Half of the patients diagnosed with hyperparathyroidismdo not have symptoms.
SUPPORTIVE THERAPYInHyperparathyroidism• Secondary hyperparathyroidism, with manifestationssimilar to those of primary hyperparathyroidism, occursin patients with chronic renal failure and so-called renalrickets as a result of phosphorus retention, increasedstimulation of the parathyroid glands, and increasedparathyroid hormone secretion.Hyperparathyroidism is most commonly causedby a tumor.
SUPPORTIVE THERAPYInClinical Manifestations• Apathy, fatigue, muscle weakness, nausea, vomiting,constipation, hypertension, and cardiac dysrhythmiasmay occur; all are attributable to the increasedconcentration of calcium in the blood.• Psychological manifestations may vary from irritabilityand neurosis to psychoses caused by the direct effect ofcalcium on the brain and nervous system.• The formation of stones in one or both kidneys, relatedto the increased urinary excretion of calcium andphosphorus, is one of the important complications ofhyperparathyroidism and occurs in 55% of patients withprimary hyperparathyroidism.
SUPPORTIVE THERAPYInClinical Manifestations• Renal damage results from the precipitation of calciumphosphate in the renal pelvis and parenchyma, resultingin renal calculi, obstruction, pyelonephritis, and renalfailure.• The patient may develop skeletal pain and tenderness,especially of the back and joints; pain on weight bearing;pathologic fractures; deformities; and shortening of bodystature.Remember: calcium acts like a sedative. Whenanswering test questions about calcium, think musclesfirst. Don’t forget the smooth muscles of the body suchas found in the airway or intestines.
SUPPORTIVE THERAPYInClinical Manifestations• Bone loss attributable to hyperparathyroidism increasesthe risk for fracture.• The incidence of peptic ulcer and pancreatitis isincreased with hyperparathyroidism and may beresponsible for many of the gastrointestinal symptomsthat occur.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• Primary hyperparathyroidism is diagnosed by persistentelevation of serum calcium levels and an elevated levelof parathormone.• Radioimmunoassays for parathormone are sensitive anddifferentiate primary hyperparathyroidism from othercauses of hypercalcemia in more than 90% of patientswith elevated serum calcium levels.• An elevated serum calcium level alone is a nonspecificfinding because serum levels may be altered by diet,medications, and renal and bone changes.• Bone changes may be detected on x-ray or bone scansin advanced disease.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• The double antibody parathyroid hormone test is used todistinguish between primary hyperparathyroidism andmalignancy as a cause of hypercalcemia.• Ultrasound, MRI, thallium scan, and fine-needle biopsyhave been used to evaluate the function of theparathyroids and to localize parathyroid cysts,adenomas, or hyperplasia.
SUPPORTIVE THERAPYInHypercalcemic Crisis• Serum calcium levels higher than 15 mg/dL (3.7 mmol/L)result in neurologic, cardiovascular, and renal symptomsthat can be life-threatening.• Treatment includes rehydration with large volumes ofintravenous fluids, diuretic agents to promote renalexcretion of excess calcium, and phosphate therapy tocorrect hypophosphatemia and decrease serum calciumlevels by promoting calcium deposit in bone andreducing the gastrointestinal absorption of calcium.• Cytotoxic agents (mithramycin), calcitonin, and dialysismay be used in emergency situations to decrease serumcalcium levels quickly.
SUPPORTIVE THERAPYInHypercalcemic Crisis• A combination of calcitonin and corticosteroids has beenadministered in emergencies to reduce the serumcalcium level by increasing calcium deposition in bone.• Other agents that may be administered to decreaseserum calcium levels include bisphosphonates (eg,etidronate [Didronel], pamidronate).• The patient requires expert assessment and care tominimize complications and reverse the life-threateninghypercalcemia.• Medications are administered with care, and attention isgiven to fluid balance to promote return of normal fluidand electrolyte balance.
SUPPORTIVE THERAPYInHypercalcemic Crisis• Supportive measures are necessary for the patient andfamily.situations to decrease serum calcium levelsquickly.
SUPPORTIVE THERAPYInMedical Management• The insidious onset and chronic nature ofhyperparathyroidism and its diverse and commonly vaguesymptoms may result in depression and frustration.• The family may have considered the patient’s illness to bepsychosomatic.• An awareness of the course of the disorder and anunderstanding approach by the nurse may help the patientand family to deal with their reactions and feelings.• The recommended treatment of primaryhyperparathyroidism is the surgical removal of abnormalparathyroid tissue.
SUPPORTIVE THERAPYInMedical Management• In some patients without symptoms and with only mildlyelevated serum calcium levels and normal renalfunction, surgery may be delayed and the patientfollowed closely for worsening of hypercalcemia, bonedeterioration, renal impairment, or the development ofkidney stones.
SUPPORTIVE THERAPYInMedical ManagementHYDRATION THERAPY• Because kidney involvement is possible, patients withhyperparathyroidism are at risk for renal calculi.• Fluid intake of 2,000 mL or more is encouraged to helpprevent calculus formation.• Cranberry juice is suggested because it may lower theurinary pH. It can be added to juices and ginger ale forvariety.• The patient is instructed to report other manifestations ofrenal calculi, such as abdominal pain and hematuria.
SUPPORTIVE THERAPYInMedical ManagementHYDRATION THERAPY• Thiazide diuretics are avoided because they decreasethe renal excretion of calcium and further elevate serumcalcium levels.• Because of the risk of hypercalcemic crisis, the patient isinstructed to avoid dehydration and to seek immediatehealth care if conditions that commonly producedehydration (eg, vomiting, diarrhea) occur.
SUPPORTIVE THERAPYInMedical ManagementMOBILITY• Mobility of the patient, with walking or use of a rockingchair for those with limited mobility, is encouraged asmuch as possible because bones subjected to normalstress give up less calcium.• Bed rest increases calcium excretion and the risk forrenal calculi.• Oral phosphates lower the serum calcium level in somepatients.• Long term use is not recommended because of the riskfor ectopic calcium phosphate deposits in soft tissues.
SUPPORTIVE THERAPYInMedical ManagementDIET AND MEDICATIONS• Nutritional needs are met, but the patient is advised toavoid a diet with restricted or excess calcium.• If the patient has a coexisting peptic ulcer, prescribedantacids and protein feedings are necessary.• Because anorexia is common, efforts are made toimprove the appetite.• Prune juice, stool softeners, and physical activity, alongwith increased fluid intake, help to offset constipation,which is common postoperatively.
SUPPORTIVE THERAPYInNursing Management• Although not all parathyroid tissue is removed duringsurgery in an effort to control the calcium–phosphorusbalance, the nurse closely monitors the patient to detectsymptoms of tetany (which may be an earlypostoperative complication).• The nurse reminds the patient and family about theimportance of follow-up to ensure return of serumcalcium levels to normal.
SUPPORTIVE THERAPYInHypoparathyroidism• The most common cause of hypoparathyroidism isinadequate secretion of parathyroid hormone afterinterruption of the blood supply or surgical removal ofparathyroid gland tissue during thyroidectomy,parathyroidectomy, or radical neck dissection.• Atrophy of the parathyroid glands of unknown cause is aless common cause of hypoparathyroidism.
SUPPORTIVE THERAPYInPathophysiology• Symptoms of hypoparathyroidism are caused by adeficiency of parathormone that results in elevated bloodphosphate (hyperphosphatemia) and decreased bloodcalcium (hypocalcemia) levels.• In the absence of parathormone, there is decreasedintestinal absorption of dietary calcium and decreasedresorption of calcium from bone and through the renaltubules.• Decreased renal excretion of phosphate causeshypophosphaturia, and low serum calcium levels resultin hypocalciuria.
SUPPORTIVE THERAPYInClinical Manifestations• Hypocalcemia causes irritability of the neuromuscularsystem and contributes to the chief symptom ofhypoparathyroidism—tetany.• Tetany is a general muscle hypertonia, with tremor andspasmodic or uncoordinated contractions occurring withor without efforts to make voluntary movements.• Symptoms of latent tetany are numbness, tingling, andcramps in the extremities, and the patient complains ofstiffness in the hands and feet.• In overt tetany, the signs include bronchospasm,laryngeal spasm, carpopedal spasm, dysphagia,photophobia, cardiac dysrhythmias and seizures.
SUPPORTIVE THERAPYInClinical Manifestations• Other symptoms include anxiety, irritability, depression,and even delirium. ECG changes and hypotension alsomay occur.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• A positive Trousseau’s sign or a positive Chvostek’ssign suggests latent tetany.• Trousseau’s sign is positive when carpopedal spasm isinduced by occluding the blood flow to the arm for 3minutes with a blood pressure cuff.• Chvostek’s sign is positive when a sharp tapping overthe facial nerve just in front of the parotid gland andanterior to the ear causes spasm or twitching of themouth, nose, and eye.• The diagnosis of hypoparathyroidism often is difficultbecause of the vague symptoms, such as aches andpains.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• Tetany develops at serum calcium levels of 5 to 6 mg/dL(1.2 to 1.5 mmol/L) or lower.• Serum phosphate levels are increased, and x-rays ofbone show increased density.• Calcification is detected on x-rays of the subcutaneousor paraspinal basal ganglia of the brain.Chvostek’s sign is unilateral contraction of facialmuscles when the cheek is tapped. Trousseau’s sign isa hand tremor in response to the pumping up of ablood pressure cuff on the same arm.
SUPPORTIVE THERAPYInMedical Management• The goal of therapy is to raise the serum calcium level to9 to 10 mg/dL (2.2 to 2.5 mmol/L) and to eliminate thesymptoms of hypoparathyroidism and hypocalcemia.• When hypocalcemia and tetany occur after athyroidectomy, the immediate treatment is to administercalcium gluconate intravenously.• If this does not decrease neuromuscular irritability andseizure activity immediately, sedative agents such aspentobarbital may be administered.• Parenteral parathormone can be administered to treatacute hypoparathyroidism with tetany.
SUPPORTIVE THERAPYInMedical Management• The high incidence of allergic reactions to injections ofparathormone, however, limits its use to acute episodesof hypocalcemia.• The patient receiving parathormone is monitored closelyfor allergic reactions and changes in serum calciumlevels.• Because of neuromuscular irritability, the patient withhypocalcemia and tetany requires an environment that isfree of noise, drafts, bright lights, or sudden movement.• Tracheostomy or mechanical ventilation may becomenecessary, along with bronchodilating medications, if thepatient develops respiratory distress.
SUPPORTIVE THERAPYInMedical Management• A diet high in calcium and low in phosphorus is prescribed.• Although milk, milk products, and egg yolk are high incalcium, they are restricted because they also contain highlevels of phosphorus.• Spinach also is avoided because it contains oxalate, whichwould form insoluble calcium substances.• Oral tablets of calcium salts, such as calcium gluconate,may be used to supplement the diet.• Aluminum hydroxide gel or aluminum carbonate (Gelusil,Amphojel) also is administered after meals to bindphosphate and promote its excretion through thegastrointestinal tract.
SUPPORTIVE THERAPYInMedical Management• Variable dosages of a vitamin D preparation—dihydrotachysterol (AT 10 or Hytakerol), ergocalciferol(vitamin D), cholecalciferol (vitamin D)—are usuallyrequired and enhance calcium absorption from thegastrointestinal tract.
SUPPORTIVE THERAPYInNursing Management• Care of postoperative patients having thyroidectomy,parathyroidectomy, and radical neck dissection is directedtoward detecting early signs of hypocalcemia andanticipating signs of tetany, seizures, and respiratorydifficulties.• Calcium gluconate is kept at the bedside, with equipmentnecessary for intravenous administration.• If the patient has a cardiac disorder, is subject todysrhythmias, or is receiving digitalis, calcium gluconate isadministered slowly and cautiously.• Calcium and digitalis increase systolic contraction and alsopotentiate each other; this may produce potentially fataldysrhythmias.
SUPPORTIVE THERAPYInNursing Management• Consequently, the cardiac patient requires continuouscardiac monitoring and careful assessment.• An important aspect of nursing care is teaching aboutmedications and diet therapy.• The patient needs to know the reason for high calciumand low phosphate intake and the symptoms ofhypocalcemia and hypercalcemia; he or she shouldknow to contact the physician immediately if thesesymptoms occur.
SUPPORTIVE THERAPYInAdrenal Disorders• There are two adrenal glands in the human, eachattached to the upper portion of a kidney.• Each adrenal gland is, in reality, two endocrine glandswith separate, independent functions.• The adrenal medulla at the center of the gland secretescatecholamines, and the outer portion of the gland, theadrenal cortex, secretes steroid hormones.• The secretion of hormones from the adrenal cortex isregulated by the hypothalamicpituitary- adrenal axis.• The hypothalamus secretes corticotropinreleasinghormone (CRH), which in turn stimulates the pituitarygland to secrete ACTH.
SUPPORTIVE THERAPYInAdrenal Disorders• ACTH then stimulates the adrenal cortex to secreteglucocorticoid hormone (cortisol).• Increased levels of the adrenal hormone then inhibit theproduction or secretion of CRH and ACTH.• This system is an example of a negative feedbackmechanism.
SUPPORTIVE THERAPYInAdrenal FunctionADRENAL MEDULLA• The adrenal medulla functions as part of the autonomicnervous system.• Stimulation of preganglionic sympathetic nerve fibers,which travel directly to the cells of the adrenal medulla,causes release of the catecholamine hormonesepinephrine and norepinephrine.• About 90% of the secretion of the human adrenalmedulla is epinephrine.• Catecholamines regulate metabolic pathways topromote catabolism of stored fuels to meet caloric needsfrom endogenous sources.
SUPPORTIVE THERAPYInAdrenal FunctionADRENAL MEDULLA• The major effects of epinephrine release are to prepareto meet a challenge (fight-or-flight response).• Secretion of epinephrine causes decreased blood flowto tissues that are not needed in emergency situations,such as the gastrointestinal tract, and causes increasedblood flow to tissues that are important for effective fightor flight, such as cardiac and skeletal muscle.• Catecholamines also induce the release of free fattyacids, increase the basal metabolic rate, and elevate theblood glucose level.
SUPPORTIVE THERAPYInAdrenal FunctionADRENAL CORTEX• A functioning adrenal cortex is necessary for life;adrenocortical secretions make it possible for the bodyto adapt to stress of all kinds.• The three types of steroid hormones produced by theadrenal cortex are glucocorticoids, the prototype ofwhich is hydrocortisone; mineralocorticoids, mainlyaldosterone; and sex hormones, mainly androgens(male sex hormones).• Without the adrenal cortex, severe stress would causeperipheral circulatory failure, circulatory shock, andprostration.
SUPPORTIVE THERAPYInAdrenal FunctionADRENAL CORTEX• Survival in the absence of a functioning adrenal cortex ispossible only with nutritional, electrolyte, and fluidreplacement and appropriate replacement withexogenous adrenocortical hormones.Many heart attacks occur during the early morninghours when people are coming out of REM sleep, asthis is a very stressful time for the body.The steroids produced by the adrenal cortex (corticalsteroids) are made from cholesterol.CHOLESTEROL IS GOOD FOR YOU!
SUPPORTIVE THERAPYInAdrenal FunctionGLUCOCORTICOIDS• The glucocorticoids are so named because they have animportant influence on glucose metabolism: increasedhydrocortisone secretion results in elevated bloodglucose levels.• Glucocorticoids are secreted from the adrenal cortex inresponse to the release of ACTH from the anterior lobeof the pituitary gland.• The presence of glucocorticoids in the blood inhibits therelease of corticotropin-releasing factor from thehypothalamus and also inhibits ACTH secretion from thepituitary.
SUPPORTIVE THERAPYInAdrenal FunctionGLUCOCORTICOIDS• The resultant decrease in ACTH secretion causesdiminished release of glucocorticoids from the adrenalcortex.• Glucocorticoids are administered frequently to inhibit theinflammatory response to tissue injury and suppressallergic manifestations.• Their side effects include the development of diabetesmellitus, osteoporosis, peptic ulcer, increased proteinbreakdown resulting in muscle wasting and poor woundhealing, and redistribution of body fat.
SUPPORTIVE THERAPYInAdrenal FunctionGLUCOCORTICOIDS• Large amounts of exogenously administeredglucocorticoids in the blood inhibit the release of ACTHand endogenous glucocorticoids.• Because of this, the adrenal cortex can atrophy.• If exogenous glucocorticoid administration isdiscontinued suddenly, adrenal insufficiency resultsbecause of the inability of the atrophied cortex torespond adequately.
SUPPORTIVE THERAPYInAdrenal FunctionMINERALOCORTICOIDS• Mineralocorticoids exert their major effects on electrolytemetabolism.• They act principally on the renal tubular andgastrointestinal epithelium to cause increased sodiumion absorption in exchange for excretion of potassium orhydrogen ions.• ACTH only minimally influences aldosterone secretion.• It is primarily secreted in response to the presence ofangiotensin II in the bloodstream.• Angiotensin II is a substance that elevates the bloodpressure by constricting arterioles.
SUPPORTIVE THERAPYInAdrenal FunctionMINERALOCORTICOIDS• Its concentration is increased when renin is releasedfrom the kidney in response to decreased perfusionpressure.• The resultant increased aldosterone levels promotesodium reabsorption by the kidney and thegastrointestinal tract, which tends to restore bloodpressure to normal.• The release of aldosterone is also increased byhyperkalemia.• Aldosterone is the primary hormone for the long-termregulation of sodium balance.
SUPPORTIVE THERAPYInAdrenal FunctionADRENAL SEX HORMONES• Androgens, the third major type of steroid hormonesproduced by the adrenal cortex, exert effects similar tothose of male sex hormones.• The adrenal gland may also secrete small amounts ofsome estrogens, or female sex hormones.• ACTH controls the secretion of adrenal androgens.When secreted in normal amounts, the adrenalandrogens probably have little effect, but when secretedin excess, in certain inborn enzyme deficiencies,masculinization may result.• This is termed the ADRENOGENITAL SYNDROME.
Major Actions and Source of HormonesADRENAL CORTEX1. Mineralocorticosteroids, mainly aldosterone• Increases sodium absorption and potassium loss bythe kidneys.2. Glucocorticoids, mainly cortisol• Affects metabolism of all nutrients; regulates bloodglucose levels, affects growth, has anti-inflammatoryaction, and decreases effects of stress
Major Actions and Source of HormonesADRENAL CORTEX3. Adrenal androgens, dehydroepiandrosterone DHEAand androstenedione• Have minimal intrinsic androgenic activity; they areconverted to testosterone and dihydrotestosterone inthe peripherySynthetic androgens (sex hormones) are referredto as anabolic steroids.
Major Actions and Source of HormonesADRENAL MEDULLA1. Epinephrine2. Norepinephrine• Serve as neurotransmitters for the sympatheticnervous system
SUPPORTIVE THERAPYInPheochromocytoma• Pheochromocytoma is a tumor that is usually benignand originates from the chromaffin cells of the adrenalmedulla.• Pheochromocytoma may occur at any age, but its peakincidence is between ages 40 and 50 years.• It affects men and women equally.• Because of the high incidence of pheochromocytoma infamily members, the patient’s family members should bealerted and screened for this tumor.
SUPPORTIVE THERAPYInPheochromocytoma• Pheochromocytoma is the cause of high blood pressurein 0.2% of patients with new onset of hypertension.• Pheochromocytoma may occur in the familial form aspart of multiple endocrine neoplasia type 2; therefore, itshould be considered a possibility in patients withmedullary thyroid carcinoma and parathyroidhyperplasia or tumor.
SUPPORTIVE THERAPYInClinical Manifestations• The nature and severity of symptoms of functioningtumors of the adrenal medulla depend on the relativeproportions of epinephrine and norepinephrinesecretion.• The typical triad of symptoms comprises headache,diaphoresis, and palpitations.• Hypertension and other cardiovascular disturbances arecommon. The hypertension may be intermittent orpersistent.• Other symptoms may include tremor, headache,flushing, and anxiety.
SUPPORTIVE THERAPYInClinical Manifestations• Hyperglycemia may result from conversion of liver andmuscle glycogen to glucose by epinephrine secretion;insulin may be required to maintain normal bloodglucose levels.• The clinical picture in the paroxysmal form ofpheochromocytoma is usually characterized by acute,unpredictable attacks lasting seconds or several hours.During these attacks, the patient is extremely anxious,tremulous, and weak.• The patient may experience headache, vertigo, blurringof vision, tinnitus, air hunger, and dyspnea.
SUPPORTIVE THERAPYInClinical Manifestations• Other symptoms include polyuria, nausea, vomiting,diarrhea, abdominal pain, and a feeling of impendingdoom.• Palpitations and tachycardia are common.• Blood pressures exceeding 250/150 mm Hg have beenrecorded. Such blood pressure elevations are life-threatening and may cause severe complications, suchas cardiac dysrhythmias, dissecting aneurysm, stroke,and acute renal failure.• Postural hypotension occurs in 70% of patients withuntreated pheochromocytoma.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• Pheochromocytoma is suspected if signs of sympatheticnervous system overactivity occur in association withmarked elevation of blood pressure.• These signs can be associated with the ―five Hs‖:hypertension, headache, hyperhidrosis,hypermetabolism, and hyperglycemia.• Measurements of urine and plasma levels ofcatecholamines are the most direct and conclusive testsfor overactivity of the adrenal medulla.• A 24-hour specimen of urine is collected for determiningfree catecholamines.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• A number of medications and foods (eg, coffee, tea,bananas, chocolate, vanilla, aspirin) may alter the resultsof these tests; therefore, careful instructions to avoidrestricted items must be given to the patient.• Total plasma catecholamine (epinephrine andnorepinephrine) concentration is measured with the patientsupine and at rest for 30 minutes.• Factors that may elevate catecholamine levels must becontrolled to obtain valid results; these factors includeconsumption of coffee or tea, use of tobacco, emotionaland physical stress, and use of many prescription andover-the-counter medications (eg, amphetamines, nosedrops or sprays, decongestant agents, andbronchodilators).
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• Normal plasma values of epinephrine are 100 pg/mL(590 pmol/L); normal values of norepinephrine aregenerally less than 100 to 550 pg/mL (590 to 3,240pmol/L).• Values of epinephrine greater than 400 pg/mL (2,180pmol/L) or norepinephrine values greater than 2,000pg/mL (11,800 pmol/L) are considered diagnostic ofpheochromocytoma.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• Imaging studies, such as CT scans, MRI, andultrasound, may also be carried out to localize thepheochromocytoma and to determine whether morethan one tumor is present.• Use of 131I-metaiodobenzylguanidine (MIBG)scintigraphy may be required to determine the locationof the pheochromocytoma and to detect metastatic sitesoutside the adrenal gland.• MIBG scintigraphy is a noninvasive, safe procedure thathas increased the accuracy of diagnosis of adrenaltumors.
SUPPORTIVE THERAPYInMedical ManagementPHARMACOLOGIC THERAPY• The patient may be moved to the intensive care unit forclose monitoring of ECG changes and carefuladministration of alphaadrenergic blocking agents (eg,phentolamine [Regitine]) or smooth muscle relaxants (eg,sodium nitroprusside [Nipride]) to lower the blood pressurequickly.• Phenoxybenzamine (Dibenzyline), a long-acting alpha-blocker, may be used when the blood pressure is stable toprepare the patient for surgery.• Beta-adrenergic blocking agents, such as propranolol(Inderal), may be used in patients with cardiacdysrhythmias or those not responsive to alpha-blockers.
SUPPORTIVE THERAPYInMedical ManagementPHARMACOLOGIC THERAPY• Alphaadrenergic and beta-adrenergic blocking agentsmust be used with caution because patients withpheochromocytoma may have increased sensitivity tothem.• Still other medications that may be used preoperativelyare catecholamine synthesis inhibitors, such as alpha-methyl-p-tyrosine (metyrosine).• These are occasionally used when adrenergic blockingagents do not reduce the effects of catecholamines.
SUPPORTIVE THERAPYInMedical ManagementSURGICAL MANAGEMENT• The definitive treatment of pheochromocytoma issurgical removal of the tumor, usually withADRENALECTOMY.• Bilateral adrenalectomy may be necessary if tumors arepresent in both adrenal glands.• Phentolamine or phenoxybenzamine (Dibenzyline) maybe used safely without causing undue hypotension.• Other medications (metyrosine [Demser] and prazosin[Minipress]) have been used to treatpheochromocytoma.
SUPPORTIVE THERAPYInMedical ManagementSURGICAL MANAGEMENT• The patient needs to be well hydrated before, during,and after surgery to prevent hypotension.• Corticosteroid replacement is required if bilateraladrenalectomy has been necessary.
SUPPORTIVE THERAPYInNursing Management• The patient who has undergone surgery to treatpheochromocytoma has experienced a stressfulpreoperative and postoperative course and may remainfearful of repeated attacks.• The patient is monitored for several days in the intensivecare unit with special attention given to ECG changes,arterial pressures, fluid and electrolyte balance, andblood glucose levels.• Several intravenous lines are inserted for administrationof fluids and medications.
SUPPORTIVE THERAPYInAdrenocortical Deficiencies• ADDISON’S DISEASE, results when adrenal cortexfunction is inadequate to meet the patient’s need forcortical hormones.• Autoimmune or idiopathic atrophy of the adrenal glandsis responsible for 80% of cases.• Other causes include surgical removal of both adrenalglands or infection of the adrenal glands.• Tuberculosis and histoplasmosis are the most commoninfections that destroy adrenal gland tissue.• Inadequate secretion of ACTH from the pituitary glandalso results in adrenal insufficiency because ofdecreased stimulation of the adrenal cortex.
SUPPORTIVE THERAPYInAdrenocortical Deficiencies• Therapeutic use of corticosteroids is the most commoncause of adrenocortical insufficiency.• Treatment with daily administration of corticosteroids for2 to 4 weeks may suppress function of the adrenalcortex; therefore, adrenal insufficiency should beconsidered in any patient who has been treated withcorticosteroids.The most common cause of Addison’s disease isan autoimmune response. The adrenal cortexloses about 90% of its function before any clinicalmanifestations appear.
SUPPORTIVE THERAPYInClinical Manifestations• Addison’s disease is characterized by muscle weakness,anorexia, gastrointestinal symptoms, fatigue,emaciation, dark pigmentation of the skin, knuckles,knees, elbows, and mucous membranes, hypotension,and low blood glucose levels, low serum sodium levels,and high serum potassium levels.• Mental status changes such as depression, emotionallability, apathy, and confusion are present in 60% to 80%of patients.• In severe cases, the disturbance of sodium andpotassium metabolism may be marked by depletion ofsodium and water and severe, chronic dehydration.
SUPPORTIVE THERAPYInClinical Manifestations• With disease progression and acute hypotension, thepatient develops ADDISONIAN CRISIS, which ischaracterized by cyanosis and the classic signs ofcirculatory shock: pallor, apprehension, rapid and weakpulse, rapid respirations, and low blood pressure.• In addition, the patient may complain of headache,nausea, abdominal pain, and diarrhea and show signs ofconfusion and restlessness.• Even slight overexertion, exposure to cold, acuteinfections, or a decrease in salt intake may lead tocirculatory collapse, shock, and death if untreated.
SUPPORTIVE THERAPYInAssessment and Diagnostic Findings• Laboratory findings include decreased blood glucose(hypoglycemia) and sodium (hyponatremia) levels, anincreased serum potassium (hyperkalemia) level, and anincreased white blood cell count (leukocytosis).• The diagnosis is confirmed by low levels ofadrenocortical hormones in the blood or urine anddecreased serum cortisol levels.• If the adrenal cortex is destroyed, baseline values arelow, and ACTH administration fails to cause the normalrise in plasma cortisol and urinary 17-hydroxycorticosteroids.
SUPPORTIVE THERAPYInMedical Management• Immediate treatment is directed toward combatingcirculatory shock: restoring blood circulation,administering fluids and corticosteroids, monitoring vitalsigns, and placing the patient in a recumbent positionwith the legs elevated.• Hydrocortisone (Solu-Cortef) is administeredintravenously, followed with 5% dextrose in normalsaline.• Vasopressor amines may be required if hypotensionpersists.• Antibiotics may be administered if infection hasprecipitated adrenal crisis in a patient with chronicadrenal insufficiency.
SUPPORTIVE THERAPYInMedical Management• Additionally, the patient is assessed closely to identifyother factors, stressors, or illnesses that led to the acuteepisode.• The patient will require additional supplementary therapywith glucocorticoids during stressful procedures orsignificant illnesses to prevent addisonian crisis.• Additionally, the patient may need to supplement dietaryintake with added salt during times of gastrointestinallosses of fluids through vomiting and diarrhea.For clients who take steroids, teach them to neverstop taking the steroid suddenly, as this couldresult in an addisonian crisis, shock, and death.