Regulate the overall metabolic rate and the storage, conversion, and release of energy.
Regulate fluid and electrolyte balance.
Initiate coping responses to stressors.
Regulate growth and development.
Regulate reproduction processes.
Hormone secretion is typically controlled through a negative feedback system.
Fall in blood concentration of hormone leads to activation of the regulator endocrine gland and to release of its stimulator hormones.
Elevations in blood concentration of target cell hormones or of changes in blood composition resulting from target cell activity can cause inhibition of hormone secretion.
Endocrine disorders are manifested as states of hormone deficiency or hormone excess. The underlying pathophysiology may be expressed as:
Primary—the secreting gland releases inappropriate hormone because of disease of the gland itself.
Secondary—the secreting gland releases abnormal amounts of hormone because of disease in a regulator gland (eg, pituitary).
Tertiary—the secreting gland releases inappropriate hormone because of hypothalamic dysfunction, resulting in abnormal stimulation by the pituitary.
Abnormal hormone concentrations may also be caused by hormone-producing tumors (adenomas) located at a remote site.
This is a direct measurement of the concentration of total thyroxine (T4) in the blood, using a radioimmunoassay technique.
It is an accurate index of thyroid function when T4-binding globulin (TBG) is normal.
Low plasma-binding protein states (malnutrition, liver disease) may give low values.
High plasma-binding protein values (pregnancy, estrogen therapy) may give high values.
It is used to diagnose hypofunction and hyperfunction of the thyroid and to guide and evaluate thyroid hormone replacement therapy.
The test to monitor thyroid hormone therapy should be performed 6 to 8 weeks after dosage adjustment because of the time required for thyroid-stimulating hormone (TSH) to reflect the body’s response to the new dose.
Interpretation of test results:
Hypothyroidism—below normal.
Hyperthyroidism—above normal.
Iodides can affect the results of thyroid tests; therefore, it is important to determine if patient has had any recent tests that used iodine as a contrast medium.
Direct measurement of free T4 concentration in the blood using a two-step radioimmunoassay method.
Accurate measure of thyroid function independent of the variable influence of thyroid-binding globulin levels.
Used to aid in the diagnosis of hyperthyroidism and hypothyroidism.
Used to monitor and guide thyroid hormone replacement therapy, particularly with pituitary disease.
Interpretation of test results:
Hyperthyroidism—above normal.
Hypothyroidism—below normal.
Results best interpreted in conjunction with TSH levels for diagnostic purposes.
When used to monitor thyroid hormone replacement therapy, levels meaningful only after 6 to 8 weeks of therapy to evaluate adequacy of dosage because of long half-life of T4.
This measures the concentration of the carrier protein for T4 in the blood.
Because most T4 is protein bound, changes in TBG will influence values of T4.
Helpful in distinguishing between true thyroid disease and T4 test abnormalities caused by TBG excess or deficit.
Directly measures concentration of triiodothyronine (T3) in the blood using a radioimmunoassay technique.
T3 is less influenced by alterations in thyroid-binding proteins.
T3 has a shorter half-life than T4 and occurs in minute quantities in the active form.
Useful to rule out T3 thyrotoxicosis, hyperthyroidism when T4 is normal, and to evaluate effects of thyroid replacement therapy.
T3 can be transiently depressed in the acutely ill patient.
Interpretation of test results:
Hypothyroidism—below normal.
Hyperthyroidism—above normal.
This is an indirect measure of thyroid function, based on the available protein-binding sites in a serum sample that can bind to radioactive T3.
The radioactive T3 is added to the serum sample in the test tube and will bind with available protein-binding sites. The unbound T3 binds to resin for T3 uptake, reflecting the amount of T3 left over because of lack of binding sites.
Estrogen and pregnancy produce an increase in binding sites, thus causing a lowered T3 resin uptake.
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Results may be altered if patient has been taking estrogens, androgens, salicylates, or phenytoin.
Interpretation of test results:
Hypothyroidism—below normal.
Hyperthyroidism—above normal.
Below normal—hypothyroidism.
Above normal—hyperthyroidism.
Direct measure of TSH, the hormone secreted by the pituitary gland that regulates the production and secretion of T4 by the thyroid gland.
Blood sample is analyzed by radioimmunoassay.
Preferred test differentiates between thyroid disorders caused by disease of the thyroid gland itself and disorders caused by disease of the pituitary or hypothalamus. Also useful to detect early stages of hypothyroidism (subclinical hypothyroidism) and to monitor hormone replacement therapy (HRT). Patient must be on a stable dose of thyroxine for 6 to 8 weeks for TSH levels to accurately reflect adequacy of treatment.
Morning samples are preferred.
Interpretation:
In primary hypothyroidism, TSH levels are elevated.
In secondary hypothyroidism (failure of the pituitary gland), TSH levels are low.
In hyperthyroidism, TSH levels are low.
The thyrotropin-releasing hormone (TRH) stimulation test evaluates the patency of the pituitary-hypothalamic axis. Once used primarily to distinguish between primary and central hypothyroidism, this test is rarely used for that purpose with the advent of more sensitive TSH assays. Now, its primary use is to distinguish between secondary and tertiary hypothyroidism and evaluate acromegaly.
A baseline sample is drawn, then TRH is administered via intravenous (IV) injection and blood samples are drawn to determine TSH levels at 30, 90, and 120 minutes.
Interpretation:
Increased TSH should be seen within 30 minutes.
No rise in secondary hypothyroidism.
Blunted rise in hyperthyroidism.
Delayed rise (90-minute sample) associated with tertiary hypothyroidism.
Elevated growth hormone levels associated with acromegaly.
A subnormal response can occur in patients taking L-dopa or cortisol.
Thyroid-stimulating immunoglobulin (TSI)—autoantibodies that stimulate the TSH receptor on the thyroid gland,
causing hyperfunction of the thyroid. Helpful in the diagnosis of Graves’ disease.
Thyroid peroxidase antibodies—associated with Hashimoto’s thyroiditis and Graves’ disease.
Thyroglobulin antibodies—elevated with Hashimoto’s thyroiditis and Graves’ disease.
Test is a direct measurement of parathyroid hormone (PTH) concentration in the blood, using radioimmunoassay technique.
Results are usually compared with results of total serum calcium to determine likely cause of parathyroid dysfunction.
Range of normal values may vary by laboratory and method.
This is a direct measurement of protein-bound and “free” ionized calcium.
Ionized calcium fraction is the best indicator of changes in calcium metabolism.
Results can be affected by changes in serum albumin, the primary protein carrier.
Used to detect alterations in calcium metabolism caused by parathyroid disease or malignancy.
Sample may be obtained from fasting patient and should be collected in tube with heparin as anticoagulant.
Test may be repeated to confirm parathyroid disease.
Elevations in serum calcium can be caused by dehydration, vitamin D intoxication, thiazide diuretics, immobilization, hyperthyroidism, or lithium therapy.
Low values may be seen in renal failure, chronic disease states, malabsorption syndrome, and vitamin D deficiency.
Interpretation of test results:
Hyperparathyroidism, malignancy—elevated.
Hypoparathyroidism—below normal.
Approximately 45% to 50% of total serum calcium is in biologically active ionized form.
This is preferred method of testing changes in calcium metabolism caused by parathyroid disease, malignancy, or neck surgery.
Sample should be collected in tube with heparin as anticoagulant.
Test should be repeated on three different occasions to confirm parathyroid disease.
Hyperparathyroidism, malignancy—elevated.
Hypoparathyroidism—below normal.
Test measures the level of inorganic phosphorus in the blood.
Alteration in parathyroid function tends to have opposite effects on calcium and phosphorus metabolism.
Used to confirm metabolic abnormalities that affect calcium metabolism.
This is a direct measure of the primary secretory product of the adrenal cortex by radioimmunoassay technique.
Serum concentration varies with circadian cycle so normal values vary with time of day and stress level of patient (8:00 A.M. levels typically double that of 8:00 P.M. levels).
Useful as an initial step to assess adrenal dysfunction, but further workup is usually necessary.
A sample collected at midnight (while the patient is asleep) that yields a result of less than 2 mcg/dL may be considered diagnostic of Cushing’s syndrome.
A fasting sample is preferred.
Blood samples should coincide with circadian rhythm with draw time indicated on laboratory slip.
Interpretation of test results:
Decreased values seen in Addison’s disease, anterior pituitary hyposecretion, and secondary hypothyroidism.
Increased values seen in hyperthyroidism, stress (eg, trauma, surgery), carcinoma, Cushing’s syndrome, hypersecretion of corticotropin by tumors (oat cell cancer), adrenal adenoma, and obesity.
Because cortisol binding globulin (CBG) is normally absent from saliva, it does not interfere with cortisol levels. Therefore, salivary cortisol can be more reliably measured without variation due to fluctuating CBG levels.
A mouth swab is collected from patient at midnight.
A result of more than 2.0 ng/mL is diagnostic for Cushing’s syndrome.
Test measures cortisol production during a 24-hour period.
Useful to establish diagnosis of hypercortisolism.
Less influenced by diurnal variations in cortisol.
Instruct patient in appropriate collection technique.
Collection jug should be kept on ice and sent to laboratory promptly when collection completed.
Interfering factors:
Elevated values—pregnancy, hormonal contraceptives, spironolactone, stress.
Recent radioisotope scans can interfere with test results.
The dexamethasone suppression test (DST) is a valuable method to evaluate adrenal hyperfunction.
Adrenal production and secretion of cortisol is stimulated by adrenocorticotropic hormone (ACTH; corticotropin) from the pituitary gland.
Dexamethasone is a synthetic steroid effective in suppressing corticotropin secretion.
In a healthy patient, the administration of dexamethasone will inhibit corticotropin secretion and will cause cortisol levels to fall below normal.
Certain drugs (rifampin, phenytoin) increase metabolic clearance of dexamethasone and may contribute to false-positive test results.
Overnight low-dose (1 mg) DST (used primarily to identify those without Cushing’s syndrome).
Administer dexamethasone 1 mg orally at 11:00 P.M.
Draw cortisol level at 8:00 A.M. before patient rises.
Expect suppressed cortisol levels (<5 mcg/dL). Test is highly sensitive when a 2-mg cut-off is used for diagnosis.
Forty-eight-hour low-dose (2 mg) DST.
Patient is instructed to take 0.5 mg of dexamethasone every 6 hours for a 2-day period.
Plasma cortisol sample is collected 9 hours after first dose is administered and again at 48 hours.
It is essential that patient have clearly written instructions for compliance with dosing and blood sampling schedule for test to be valid.
High-dose overnight DST (helpful to distinguish Cushing’s disease from other forms of Cushing’s syndrome).
Give patient dexamethasone 8 mg orally at 11:00 P.M.
Draw cortisol level at 8:00 A.M. before patient rises.
Suppressed cortisol levels (less than 50% of baseline value) indicative of patient with corticotropin-secreting pituitary adenoma (Cushing’s disease).
Unsuppressed cortisol levels are associated with ectopic corticotropin secretion (malignancy) or adrenal tumors.
Encourage patient to take dexamethasone with milk because it may cause gastric irritation.
ACTH stimulates the production and secretion of cortisol by the adrenal cortex.
Demonstrates the ability of the adrenal cortex to respond appropriately to ACTH.
This is an important test to evaluate adrenal insufficiency, but may not distinguish primary insufficiency from secondary insufficiency.
Obtain baseline cortisol level.
Administer 0.25 mg ACTH (cosyntropin IV or intramuscularly [I.M.]).
Collect cortisol levels at times ordered (usually at 30 and 60 minutes).
Interpretation of test results:
Range of normal responses may vary; however, typically a rise in cortisol of double baseline value is considered normal.
Diminished response—adrenal insufficiency with low cortisol values.
Test measures responsiveness of pituitary gland to corticotropin-releasing hormone (CRH)—a hypothalamic hormone that regulates pituitary secretion of ACTH.
Useful to differentiate the cause of excess cortisol secretion when ectopic source of ACTH is suspected.
In general, CRH will stimulate ACTH secretion in the pituitary, but not in nonpituitary corticotropin-secreting tissues.
Describe procedure to patient.
Patient is given CRH (1 mcg/kg or 100 mcg) via IV line.
Catheters are advanced through the femoral veins to areas near the adrenal glands, so sampling can take place near ACTH secretion.
Blood samples for ACTH test are collected at 2, 5, 10, and 15 minutes.
Normal response is a rise in ACTH to at least double the baseline value.
Interpretation of test results:
Brisk rise in ACTH double baseline value—Cushing’s disease.
No response in ACTH—corticotropin-independent Cushing’s syndrome (adrenal tumor) or ectopic source of corticotropin secretion (ectopic tumor).
Test can produce false-negative response.
Direct measure of metabolites of catecholamines secreted by the adrenal medulla.
Metanephrine is a more reliable measure of catecholamine secretion.
Preferred method to diagnose pheochromocytoma.
Obtain proper urine collection jug with hydrochloride preservative and explain 24-hour urine collection to patient.
A wide range of medications and foods may alter test performed by some laboratories. Verify with the laboratory and health care provider the need to hold some medications, such as sympathomimetics and methyldopa, and such foods as coffee, tea, vanilla extract, and bananas before and during urine collection.
Interpretation—pheochromocytoma: vanillylmandelic acid greater than 10 mcg/mg of creatinine or greater than 10 mg/24 hours; metanephrine greater than 0.7 mcg/mg of creatinine or greater than 0.7 mg/24 hours.
Collect sample from IV catheter 20 to 30 minutes after venipuncture, if possible, to reduce the rise in catecholamine levels from pain and anxiety.
Collect the sample in a heparinized tube.
Interpretation—levels higher than 2,000 ng/L diagnostic for pheochromocytoma.
Based on the principle that catecholamine production by pheochromocytomas is autonomous, as opposed to other causes of excess catecholamines, which are regulated by the sympathetic nervous system.
Clonidine, as a central alpha-adrenergic agonist, suppresses production of catecholamines.
Useful to differentiate pheochromocytoma from essential hypertension when test results are inconclusive.
Collect baseline catecholamine sample from IV catheter 20 to 30 minutes after venipuncture, if possible, to reduce the rise in catecholamine levels from pain and anxiety.
Give clonidine 0.3 mg orally.
After 3 hours, collect second catecholamine sample.
Interpretation—in patients without pheochromocytoma, a significant drop in catecholamines should be seen at 3 hours (less than 500 pg/mL or reduction of total catecholamines by 50%), whereas in patients with pheochromocytoma, no drop in catecholamines will be evident.
Direct measure, using radioimmunoassay technique, of aldosterone, a hormone secreted by the adrenal cortex that regulates renal control of sodium and potassium.
May be measured in the blood or in 24-hour urine collection specimen.
Urine test is more reliable because it is less influenced by short-term fluctuations in the bloodstream.
Useful to diagnose primary aldosteronism.
Test results can be elevated by stress, strenuous exercise, upright posture, and medications such as diazoxide, hydralazine, and nitroprusside.
Test results may be decreased by excessive licorice ingestion and the medication, fludrocortisone and propranolol.
Direct radioimmunoassay measurement of human growth hormone (GH), secreted by the anterior pituitary gland; useful to diagnose acromegaly, gigantism, pituitary tumors, pituitaryrelated growth failure in children, or GH deficiency in adults.
Because GH secretion is episodic, single fasting samples may not be reliable to detect GH excess or deficiency.
These conditions are best evaluated by using a stimulation test (for deficiency states) or a suppression test (for hormone excess conditions).
Blood sample is taken after an overnight fast (caloric intake will lower GH blood levels).
Patient should be restful and calm before blood sample collection.
Normal range: males—less than 5 ng/mL; females—less than 8 ng/mL.
May be elevated by the following medications: alcohol, L-dopa, hormonal contraceptives, alpha-antagonists, and beta-adrenergic blockers.
Blood sample is taken after an overnight fast.
Normal values: men—1 to 20 ng/mL; women—1 to 25 ng/mL.
Values above 300 ng/mL highly suggestive of pituitary tumor.
Elevated values may be caused by exercise or by breast stimulation, such as from friction.
Medications that will elevate test results include phenothiazines, reserpine, estrogens, tricyclic antidepressants, methyldopa, antihypertensive medications, and selective serotonin reuptake inhibitors.
Direct measurement of ACTH concentration in the bloodstream by radioimmunoassay technique.
One measure of pituitary gland function useful to provide important information regarding adrenal gland dysfunction.
Useful to identify cause of adrenal abnormalities when compared with serum cortisol levels.
Because ACTH is rapidly degraded, blood samples should be centrifuged and frozen promptly to avoid falsely low results.
High stress levels in patient can invalidate results.
Interpretation of test results:
Elevated levels with elevated cortisol—Cushing’s disease or ectopic production of ACTH.
Elevated levels with low cortisol—Addison’s disease.
Low levels with elevated cortisol—adrenal tumor.
Low levels with low cortisol—hypopituitarism.
Dynamic test measures pituitary response to induced hypoglycemia, particularly GH secretion and ACTH-stimulated cortisol production by the adrenal gland.
Useful to diagnose functional hypopituitarism that is caused by pituitary disease or that appears after pituitary surgery.
Considered the “gold standard” for diagnosis of GH deficiency.
After overnight fast, insulin 0.1 unit/kg body weight is given via IV line.
Blood samples are collected, usually at baseline, 30, 60, and 90 minutes after insulin dose.
The test is considered valid if blood glucose falls to half of baseline or less than 40 mg/dL.
Peak response is seen at 60 to 100 minutes.
For adrenal response, a rise in cortisol by a factor of at least 1.5 is necessary to show normal response.
GH deficiency is present if growth hormone levels fail to rise above 3 mcg/L.
This test is contraindicated in people with epilepsy or heart disease. In people with suspected adrenal insufficiency, ACTH stimulation test should be done first.
For people in whom the insulin tolerance test is contraindicated, other agents may be used, such as clonidine, arginine, glucagon, L-dopa, or GH-releasing hormone, to stimulate GH secretion.
Patient should fast for this test.
Seventy-five to 100 g of concentrated glucose is administered by mouth.
Blood samples are collected at baseline, 30, and 60 minutes.
Interpretation of test results:
GH levels less than 2 mcg/L are considered normal.
GH levels that are not suppressed are suggestive of acromegaly.
Failure of GH suppression may also be caused by starvation or protein calorie restriction.
Patients may complain of nausea after ingesting Glucola.
Functional test of the adequacy of posterior pituitary secretion of antidiuretic hormone (ADH) and its ability to concentrate urine and to maintain serum osmolality in the face of water deprivation.
Useful to determine the diagnosis and etiology of diabetes insipidus (DI).
The test is begun by obtaining patient’s weight, serum, and urine osmolality at time 0.
Patient weight, urine output volume, and osmolality are determined hourly.
Deprivation is continued until urine osmolality “plateaus,” as evidenced by a change of less than 10% in urine osmolality between consecutive measurements and a 2% reduction in patient’s body weight. At this time, samples are collected for serum sodium, osmolality, and vasopressin.
The test may be stopped if patient loses more than 3% of his or her body weight or if cardiac instability occurs.
If urine osmolality remains below that of serum (usually 300 mOsm/kg), the diagnosis of DI is confirmed and the second stage of the test, which distinguishes central and nephrogenic DI, is begun.
Artificial ADH (desmopressin acetate [DDAVP]) 2 mcg is given SubQ or I.M. to determine changes in urine osmolality at 30, 60, and 120 minutes in response to the injected hormone.
If the highest urine osmolality value obtained after injection is more than 50% higher than the preinjection value, DI is caused by pituitary failure. If the osmolality value is less than 50% of preinjection value, then DI is caused by renal disease.
A solution of sodium iodide 131 (131I) is administered orally to fasting patient.
After a prescribed interval, usually 24 hours, measurements of radioactive counts per minute are taken with a scintillator.
Normal thyroid will remove 15% to 50% of the iodine from the bloodstream.
Hyperthyroidism may result in the removal of as much as 90% of the iodine from the bloodstream (eg, Graves’ disease); it may also cause a low uptake with some forms of thyroiditis.
Hypothyroidism—reflected in low uptake.
Rapid imaging of thyroid tissue, particularly suspicious nodules, as contrast imaging agent is rapidly taken up by functioning tissue.
Useful to diagnose thyroid carcinoma.
Contrast media is usually administered via IV line.
Technetium (99mTc) pertechnetate or 123I is used for best images.
Images can be obtained from gamma counter within 20 to 60 minutes.
May interfere with serum radioimmunoassay tests; contact laboratory to determine when blood test can be done.
Benign adenomas may be visualized as “hot” nodules, indicating increased uptake of iodine, or as “cold” nodules, indicating decreased uptake.
Malignant nodules usually take the form of “cold” nodules.
Concerned with sodium and water retention and potassium excretion.
Example—aldosterone and 11-desoxycorticosterone.
Monitor closely for electrolyte imbalance—sodium, potassium, chloride, bicarbonate—by checking laboratory test results, changes in the electrocardiogram pattern, and signs of particular excess or deficit (see Chapter 21, page 797).
Check fingerstick or serum glucose periodically for patients on corticosteroids or for patients with adrenal disease; watch for signs of hyperglycemia (polydipsia, polyphagia, polyuria, blurred vision) or hypoglycemia (nervousness, tremor, difficulty concentrating, lethargy).
Monitor for hypocalcemia after thyroidectomy, parathyroidectomy, or with hypoparathyroidism by checking serum calcium and phosphorus levels; watch for muscular twitching, anxiety, apprehension, spasms, and tetany. Check Chvostek’s sign and Trousseau’s sign.
Monitor vital signs for heart rate, BP, and presence of arrhythmias.
Monitor temperature and respiratory rate changes in thyroid and adrenal disease.
Monitor intake and output, weight changes, and edema.
Maintain a calm, quiet environment and provide meticulous care to prevent infection or dehydration in patients with adrenal hypofunction or patients on corticosteroid replacement.
After surgery, check for bleeding, signs of infection, changes in vital signs. Monitor respiratory status carefully after thyroidectomy.
Report worsening condition or development of suspicious signs and symptoms promptly to prevent serious complications, such as myxedema coma, thyroid storm, hypocalcemic tetany, adrenal crisis.
Provide support and explain care slowly and repeatedly because patient may have mental slowness, confusion, or lethargy due to his or her condition. Ask patient to restate important information to verify understanding.
Concerned with metabolic effects, including carbohydrate metabolism.
Example—cortisol.
Antagonize action of insulin; promote gluconeogenesis, which provides glucose.
Increase breakdown of protein (inhibit protein synthesis).
Increase breakdown of fatty acids.
Suppress inflammation, inhibit scar formation, block allergic responses.
Decrease number of circulating eosinophils and leukocytes; decrease size of lymphatic tissue.
Exert a permissive action (allow the full effects) on catecholamines.
Exert a permissive action on functioning of central nervous system (CNS).
Inhibit release of adrenocorticotropin.
In summary, glucocorticoids are necessary to resist noxious stimuli and environmental change.
Physiologically—to correct deficiencies or malfunction of a particular endocrine organ or system (eg, Addison’s disease).
Diagnostically—to determine proper functioning of the endocrine system.
Pharmacologically—to treat the following:
Asthma and obstructive lung disease.
Acute rheumatic fever.
Blood conditions, such as idiopathic thrombocytopenic purpura, leukemia, hemolytic anemia.
Allergic conditions—allergic rhinitis, anaphylaxis (after epinephrine).
Dermatologic problems—drug rashes, contact dermatitis, atopic dermatitis.
Ocular diseases—conjunctivitis, uveitis.
Connective tissue disorders—systemic lupus erythematosus, rheumatoid arthritis.
GI problems—ulcerative colitis.
Organ transplant recipients—as an immunosuppressive agent.
Neurologic conditions—cerebral edema, multiple sclerosis.
Determine contraindications/precautions for such therapy.
Peptic ulcer.
Diabetes mellitus.
Viral infections.
Administer a tuberculin test, if indicated, before therapy because steroids may suppress response to the test.
Assess the patient’s own level of steroid secretion, if possible.
Explain the nature of the therapy, what is required of the patient, how long therapy will last, adverse effects to watch for, and answer any questions.
May be given by various methods—orally, parenterally, sublingually, rectally, by inhalation, or by direct application to skin or mucous membrane.
Combinations of steroids with other drugs should be avoided.
To help avoid steroid adverse effects, alternate-day therapy may be used; dose is taken in the morning.
May be given in initial high doses, then reduced; if the patient has been taking steroids for several weeks, doses must be tapered gradually to prevent addisonian crisis.
Steroids may affect the circulating blood, resulting in decreased eosinophils and lymphocytes, increased red cells, and increased incidence of thrombophlebitis and infection.
Encourage the patient to avoid crowds and the possibility of exposure to infection.
Encourage exercise to prevent venous stasis.
Be aware that signs of infection/inflammation may be masked—fever, redness, swelling.
Practice and encourage good handwashing technique and asepsis.
Determine whether the patient needs assistance in dietary control. Steroids may cause weight gain and an increase in appetite.
Encourage a high-protein diet. Because steroids affect protein metabolism, there may be negative nitrogen balance.
Encourage the patient to take steroids with milk or with food. Because steroids increase secretion of gastric acid and have an inhibiting effect on secretion of mucus in the stomach, they may cause peptic ulcer.
Be on guard for early evidence of gastric hemorrhage, such as melena, blood in vomitus.
Check fasting blood glucose levels.
Steroids precipitate gluconeogenesis and insulin antagonism, which results in hyperglycemia, glucosuria, decreased carbohydrate tolerance.
Temporary insulin injections may be necessary.
Be on the alert for the possibility of pathologic fractures. Stress safety measures to prevent injury.
Steroids affect the musculoskeletal system, causing potassium depletion and muscular weakness.
Steroids cause increased output of calcium and phosphorus, which may lead to osteoporosis.
Administer a diet high in calcium and protein.
Recommend activities of daily living (ADLs) and weightbearing program; recommend normal range of motion and safe repositioning for those that are bedridden.
Restrict sodium intake and increase potassium intake.
Mineralocorticoids differ from other steroids, resulting in sodium retention and potassium depletion; edema, weight gain.
Lemon juice is high in potassium and low in sodium.
Avoid saline as a diluent in preparing injectable medications.
Check BP frequently and weigh the patient daily.
Observe for edema.
Watch for convulsive seizures (especially in children). Steroids may alter behavior patterns, increase excitability, and may affect the CNS.
Avoid overstimulating situations.
Recognize and report any mood that deviates from the usual behavior patterns.
Report unusual behavior, haunting dreams, withdrawal, or suicidal tendencies.
Recommend that the patient carry an identification card that indicates steroid therapy and name of health care provider.
Be aware that steroids affect the hypothalamic-pituitary-adrenal system, which affects the patient’s ability to respond to stress.
Advise the patient to avoid extremes of temperature, infections, and upsetting situations.
Instruct the patient to avoid injury; stress safety precautions. Because steroids interfere with fibroblasts and granulation tissue, altered response to injury results in impaired growth and delayed healing.
Observe daily the healing process of wounds, particularly surgical wounds, to recognize the potential for wound dehiscence.
Teach patient that steroids are valuable and useful medications, but that if taken for longer than 2 weeks, they may produce certain adverse effects.
Acceptable adverse effects may include weight gain (due to increased appetite and water retention), acne, headaches, fatigue, and increased urinary frequency.
Unacceptable adverse effects that are to be reported to the health care provider include dizziness when rising from chair or bed (orthostatic hypotension indicative of adrenal insufficiency), nausea, vomiting, thirst, abdominal pain, or pain of any type.
Additional reportable adverse effects include convulsive seizures, feelings of depression or nervousness, or development of an infection.
Advise patient that a fall or an automobile accident may precipitate adrenal failure. This requires an immediate injection of hydrocortisone phosphate.
Tell patients on long-term therapy that they should wear a MedicAlert bracelet and carry a kit with hydrocortisone, as prescribed.
Instruct patient to inform any physician, dentist, or nurse about steroid therapy.
Tell patient that regular follow-up visits to health care provider are required.
No special patient preparation activities are necessary for this procedure.
The procedure is explained to patient and consent is obtained.
Patient is positioned comfortably on an examination table in the supine position with the neck fully exposed.
A rolled towel or sheet is placed beneath the patient’s shoulder to hyperextend the neck, allowing ease of access to the biopsy site.
The biopsy site area is cleaned with alcohol and/or an antibacterial cleaning agent.
One percent lidocaine may be injected intracutaneously for local anesthetic to promote patient comfort.
A 25G needle is inserted into the thyroid nodule and manipulated by the physician until a small amount of bloody material is seen on the hub of the needle.
The needle is removed and attached to a syringe. The contents of the needle are expressed onto a clean glass slide. A second slide is placed on top of the first slide and then pulled apart quickly to create a thin smear.
The slides are placed in a fixative and transported to a cytologist for interpretation.
The biopsy site may be dressed with an adhesive bandage or other small dressing.
Follow-up visit for patient should be arranged to discuss results.
Prevent infection by making sure that biopsy area is prepped appropriately before procedure.
Employ comfort measures during procedure, as necessary.
Assure patient that most thyroid nodules are determined to be benign and that most thyroid malignancies have a high cure rate.
Advise patient that some soreness at the biopsy site should be expected for a brief time.
Make sure that patient follows up for results and definitive treatment.
Thyroidectomy can be total (removal of the entire thyroid gland); subtotal (95% of gland removed)—to prevent damage to the parathyroid glands; and partial (one lobe or isthmus removed)—to treat nodular disease.
The parathyroid glands are usually spared to prevent hypocalcemia.
Indications for thyroidectomy include Graves’ disease refractory to 131I therapy, large goiters, adenoma (thyroid cancer), and some nodules.
The patient must be euthyroid at time of surgery, so thioamides are administered to control hyperthyroidism.
Iodide is given to increase firmness of thyroid gland and to reduce its vascularity after blood loss.
An attempt is made to counteract the effects of hypermetabolism by maintaining a restful and therapeutic environment and by providing a nutritious diet.
The patient is prepared for surgery physically and emotionally in the following ways:
Make a special effort to ensure that patient has a good night’s rest preceding surgery.
Explain to patient that speaking is to be minimized immediately postoperatively and that oxygen may be administered to facilitate breathing.
Explain that postoperatively, fluids may be given via IV line to maintain fluid, electrolyte, and nutritional needs; IV glucose may also be given in the hours before the administration of anesthetic agents.
The patient is monitored for bleeding and respiratory distress that indicates laryngeal edema, secondary to swelling in the area of surgery.
Signs of hypocalcemia are watched for—irritability, twitching, spasms of hands and feet.
Calcium levels are monitored. If in 48 hours level falls below 7 mg/100 mL (3 mEq), IV calcium (gluconate, lactate) replacement is given.
IV calcium is used cautiously in patients who have renal disease or who are taking digoxin.
Thyroid function is monitored after surgery.
Hemorrhage, edema of the glottis, damage to laryngeal nerve.
Hypothyroidism following subtotal thyroidectomy occurs in 5% of patients in first postoperative year; increases at rate of 2% to 3% per year.
Hypoparathyroidism occurs in about 4% of patients and is usually mild and transient; requires calcium supplements via IV administration and orally when more severe.
Risk for Injury related to invasive procedure of the neck.
Risk for Injury related to possible removal of parathyroid glands.
Administer humidified oxygen, as prescribed, to reduce irritation of airway and to prevent edema.
Move patient carefully; provide adequate support to the head so that no tension is placed on the sutures.
Place patient in semi-Fowler’s position, with the head elevated and supported by pillows; avoid flexion of neck.
Monitor vital signs frequently, watching for tachycardia and hypotension that indicates hemorrhage (most likely between 12 and 24 hours postoperatively).
Observe for bleeding at sides and back of the neck, and anteriorly, when patient is in dorsal position.Stay updated, free articles. Join our Telegram channel
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