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  1. DIABETES: heterogeneous group of diseases involving the disruption of the metabolism of carbohydrates, fats, and protein. If uncontrolled, serious vascular and neurological changes occur.
    1. Types:
      1. Type 1: formerly called insulin-dependent diabetes mellitus (IDDM); and also formerly called "juvenile-onset diabetes." Insulin is needed to prevent ketosis; onset usually in youth but may occur in adulthood; prone to ketosis, unstable diabetes.
      2. Type 2: formerly called non–insulin-dependent diabetes mellitus (NIDDM); and also formerly called "maturity-onset diabetes" or "adult-onset diabetes." May be controlled with diet and oral hypoglycemics or insulin; client less apt to have ketosis, except in presence of infection. May be further classified as obese type 2 or nonobese type 2.
      3. Type 3: gestational diabetes mellitus (GDM):glucose intolerance during pregnancy in women who were not known to have diabetes before pregnancy; will be reclassified after birth; may need to be treated or may return to prepregnancy state and need no treatment.
      4. Type 4: diabetes secondary to another condition, such as pancreatic disease, other hormonal imbalances, or drug therapy such as receiving glucocorticoids.
    2. Pathophysiology:
      1. Type 1—absolute deficiency of insulin due to destruction of pancreatic beta cells by the interaction of genetic, immunological, hereditary, or environmental factors.
      2. Type 2—relative deficiency of insulin due to:
        1. An islet cell defect resulting in a slowed or delayed response in the release of insulin to a glucose load; or
        2. Reduction in the number of insulin receptors from continuously elevated insulin levels; or
        3. A postreceptor defect; or
        4. A major peripheral resistance to insulin induced by hyperglycemia. These factors lead to deprivation of insulin-dependent cells → a marked decrease in the cellular rate of glucose uptake, and therefore elevated blood glucose.
    3. Risk factors:
      1. Obesity.
      2. Family history of diabetes.
      3. Age 45 or older.
      4. Women whose babies at birth weighed more than 9 lb.
      5. History of autoimmune disease.
      6. Members of high-risk ethnic group (African American, Latino, or Native American).
      7. History of gestational diabetes mellitus.
      8. Hypertension.
      9. Elevated high-density lipoprotein (HDL).
    4. Assessment:
      1. Subjective data:
        1. Eyes: blurry vision.
        2. Skin: pruritus vulvae.
        3. Neuromuscular: paresthesia, peripheral neuropathy, lethargy, weakness, fatigue, increased irritability.
        4. GI: polydipsia (increased thirst).
        5. Reproductive: impotence.
      2. Objective data:
        1. Genitourinary: polyuria, glycosuria, nocturia (nocturnal enuresis in children).
        2. Vital signs:
          1. Pulse and temperature: normal or elevated.
          2. BP: normal or decreased, unless complications present.
          3. Respirations: increased rate and depth (Kussmaul's respirations).
        3. GI:
          1. Polyphagia, dehydration.
          2. Weight loss, failure to gain weight.
          3. Acetone breath.
        4. Skin: cuts heal slowly; frequent infections, foot ulcers, vaginitis.
        5. Neuromuscular: loss of strength, peripheral neuropathy.
        6. Laboratory data:
          1. Elevated:
            1. Blood sugar greater than 126 mg/dL fasting or 200 mg/dL 1 to 2 hours after eating.
            2. Glucose tolerance test.
            3. Glycosuria (>170 mg/100 mL).
            4. Potassium (>5 mg/dL) and chloride (>145 mg/dL).
            5. Hemoglobin A1c greater than 7%.
          2. Decreased:
            1. pH (<7.4).
            2. PaCO2 (<32).
        7. Long-term pathological considerations:
          1. Cataract formation and retinopathy: thickened capillary basement membrane, changes in vascularization and hemorrhage, due to chronic hyperglycemia.
          2. Nephropathy: due to glomerulosclerosis, arteriosclerosis of renal artery and pyelonephritis, progressive uremia.
          3. Neuropathy: due to reduced tissue perfusion; affecting motor, sensory, voluntary, and autonomic functions.
          4. Arteriosclerosis: due to lesions of the intimal wall.
          5. Cardiac: angina, coronary insufficiency, myocardial infarction.
          6. Vascular changes: occlusions, intermittent claudication, loss of peripheral pulses, arteriosclerosis.
    5. Analysis/nursing diagnosis:
      1. Altered nutrition, less than body requirements, related to inability to metabolize nutrients and weight loss.
      2. Altered nutrition, more than body requirements, related to excessive glucose intake.
      3. Risk for injury related to complications of uncontrolled diabetes.
      4. Body image disturbance related to long-term illness.
      5. Knowledge deficit (learning need) related to management of long-term illness and potential complications.
      6. Ineffective individual coping related to inability to follow diet/medication regimen.
      7. Sexual dysfunction related to impotence from diabetes and treatment.
    6. Nursing care plan/implementation:
      1. Goal: obtain and maintain normal sugar balance.
        1. Monitor: vital signs; blood glucose before meals, at bedtime, and as symptoms demand (urine testing for glucose levels is not as accurate as capillary blood testing).
        2. Medications:
          1. Oral hypoglycemics:
            1. Sulfonylureas; tolbutamide (Orinase), chlorpropamide (Diabenese), tolazamide (Tolinase), acetohexamide (Dymelor), glimepiride (Amaryl), glyburide (DiaBeta and Micronase), and glipizide (Glucocotrol).
            2. Others: metformin (Glucophage) increases body's sensitivity to insulin. Acarbose (Precose) inhibits cells of the small intestine from absorbing complex carbohydrates.
          2. Insulin (biosynthetic human insulin): bolus insulin—released in response to meals; basal insulin—released between meals, at nighttime.
            1. Rapid-acting bolus analogue of human insulin (Lispro, Aspart).
            2. Short-acting bolus (crystalline, regular) (Humulin R).
            3. Intermediate-acting basal (Lente and NPH).
            4. Slow acting (protamine zinc).
            5. Long, extended-acting basal (Ultralente).
            6. Long-acting basal analogue (Glargine).
          3. Methods of administration:
            1. Subcutaneous injection.
            2. Prefilled injectable insulin pens (Novopen and Novolin).
            3. Continuous subcutaneous insulin infusion therapy (insulin pumps).
        3. pillImageDiet, as ordered.
          1. Carbohydrate, 50% to 60%; protein, 20%; fats, 30% (saturated fats limited to 10%, unsaturated fats, 90%).
          2. Calorie reduction in adults who are obese; enough calories to promote normal growth and development for children or adults who are not obese.
          3. Limit refined sugars.
          4. Add vitamins, minerals as needed for well-balanced diet.
        4. Monitor for signs of acute (hypoglycemia, ketoacidosis) or chronic (circulatory compromise, neuropathy, nephropathy, retinopathy) complications.
      2. Goal: health teaching:
        1. Diet: foods allowed, restricted, substitutions.
        2. Medications: administration techniques, importance of using room-temperature insulin and rotating injection sites to prevent tissue damage.
        3. Desired and side effects of prescribed insulin type; onset, peak, and duration of action of prescribed insulin.
        4. Blood glucose testing techniques.
        5. Signs of complications (Table 6.28. Comparison of Diabetic Complications).
        6. Importance of health maintenance:
          1. Infection prevention, especially foot and nail care.
          2. Routine checkups.
          3. Maintain stable balance of glucose by carefully monitoring glucose level and making necessary adjustments in diet and activity level; seeking medical attention when unable to maintain balance; regular exercise program.
    7. Evaluation/outcome criteria:
      1. Optimal blood-glucose levels achieved.
      2. Ideal weight maintained.
      3. Adequate hydration.
      4. Carries out self-care activities: blood testing, foot care, exchange diets, medication administration, exercise.
      5. Recognizes and treats hyperglycemic or hypoglycemic reactions.
      6. Seeks medical assistance appropriately.
  2. NONKETOTIC HYPERGLYCEMIC HYPEROSMOLAR COMA (NKHHC): profound hyperglycemia and dehydration without ketosis or ketoacidosis; seen in type 2 diabetes; brought on by infection or illness. This condition may lead to impaired consciousness and seizures. The client is critically ill. Mortality rate is over 50%.
    1. Pathophysiology: hyperglycemia greater than 1,000 mg/dL causes osmotic diuresis, depletion of extracellular fluid, and hyperosmolarity related to infection or another stressor as the precipitating factor. Client unable to replace fluid deficits with oral intake.
    2. Risk factors:
      1. Old age.
      2. History of non–insulin-dependent diabetes.
      3. Infections: pneumonia, pyelonephritis, pancreatitis, gram-negative infections.
      4. Kidney failure: uremia and peritoneal dialysis or hemodialysis.
      5. Shock:
        1. Lactic acidosis related to bicarbonate deficit.
        2. Myocardial infarction.
      6. Hemorrhage:
        1. GI.
        2. Subdural.
        3. Arterial thrombosis.
      7. Medications:
        1. Diuretics.
        2. Glucocorticoids.
      8. Tube feedings.
    3. Assessment:
      1. Subjective data:
        1. Confusion.
        2. Lethargy.
      2. Objective data:
        1. Nystagmus.
        2. Dehydration.
        3. Aphasia.
        4. Nuchal rigidity.
        5. Hyperreflexia.
        6. Laboratory data:
          1. Blood glucose level greater than 1,000 mg/dL.
          2. Serum sodium and chloride—normal to elevated.
          3. BUN greater than 60 mg/dL (higher than in ketoacidosis because of more severe gluconeogenesis and dehydration).
          4. Arterial pH—slightly depressed.
    4. Analysis/nursing diagnosis:
      1. Risk for injury related to hyperglycemia.
      2. Altered renal peripheral tissue perfusion related to vascular collapse.
      3. Ineffective airway clearance related to coma.
    5. Nursing care plan/implementation:
      1. Goal: promote fluid and electrolyte balance.
        1. pillImageIVs: fluids and electrolytes, sodium chloride solution used initially to combat dehydration. Rate of infusion will be determined by: BP assessment, cardiovascular status, balance between fluid input and output, and laboratory values.
        2. Monitor I&O because of the high volume of fluid replaced in the critical stage of this condition.
        3. Administer nursing care for the problem that precipitated this serious condition.
        4. foodImageDiet: Food by mouth when client is able.
      2. Goal: prevent complications.
        1. pillImageAdminister regular insulin (initial dose usually 5 to 15 units) and food, as ordered.
        2. Uncontrolled condition leads to: cardiovascular disease, renal failure, blindness, and diabetic gangrene.
    6. Evaluation/outcome criteria:
      1. Blood sugar returns to normal level of 80 to 120 mg/dL.
      2. Client is alert to time, place, and person.
      3. Primary medical problem resolved.
      4. Client recognizes and reports signs of imbalance.
  3. pillImageHYPERTHYROIDISM (also called thyrotoxicosis; Graves' disease): spectrum of symptoms of accelerated metabolism caused by excessive amounts of circulating thyroid hormone. Graves' disease is most common cause of hyperthyroidism. The three components of Graves' disease are: (1) hyperthyroidism, (2) ophthalmopathy (protrusion of the eyes), and (3) skin lesions (dermopathy). Graves' disease is triggered by: stress, smoking, radiation of the neck, some medications (interleukin-2), and infections. Treatment of hyperthyroidism is accomplished by antithyroid medications, radioactive iodine administration (capsule given once), or surgery. Clients may need to take supplemental thyroid hormone (levothyroxine) after treatment.
    1. Pathophysiology: diffuse hyperplasia of thyroid gland → overproduction of thyroid hormone and increased blood serum levels. Hormone stimulates mitochondria to increase energy for cellular activities and heat production. As metabolic rate increases, fat reserves are utilized, despite increased appetite and food intake. Cardiac output is increased to meet increased tissue metabolic needs, and peripheral vasodilation occurs in response to increased heat production. Neuromuscular hyperactivity → accentuation of reflexes, anxiety, and increased alimentary tract mobility. Graves' disease is caused by stimulation of the gland by immunoglobulins of the IgG class.
    2. Risk factors:
      1. Possible autoimmune response resulting in increase of a gamma globulin called long-acting thyroid stimulator (LATS).
      2. Occurs in third and fourth decade.
      3. Affects women more than men.
      4. Emotional trauma, infection, increased stress.
      5. Overdose of medications used to treat hypothyroidism.
      6. Use of certain weight-loss products.
      7. Radiation of neck.
    3. Assessment:
      1. Subjective data:
        1. Nervousness, mood swings.
        2. Palpitations.
        3. Heat intolerance.
        4. Dyspnea.
        5. Weakness.
      2. Objective data:
        1. Eyes: exophthalmos, characteristic stare, lid lag.
        2. Skin:
          1. Warm, moist, velvety.
          2. Increased sweating; increased melanin pigmentation.
          3. Pretibial edema with thickened skin and hyperpigmentation.
        3. Weight: loss of weight despite increased appetite.
        4. Muscle: weakness, tremors, hyperkinesia.
        5. Vital signs: BP—increased systolic pressure, widened pulse pressure; tachycardia.
        6. Goiter: thyroid gland noticeable and palpable.
        7. Gynecological: abnormal menstruation.
        8. GI: frequent bowel movements.
        9. Activity pattern: overactivity leads to fatigue, which leads to depression, which stimulates client into overactivity, and pattern continues. Danger: total exhaustion.
        10. Laboratory data:
          1. Elevated: serum thyroxine (T4) (>11 mcg/100 mL), free T4 or free T4 index, triiodothyronine (T3) level (>35%) and free T3 level.
          2. Elevated: radioactive iodine uptake (RAIU) by thyroid.
          3. Elevated: basal metabolic rate (BMR).
          4. Decreased: WBC count caused by decreased granulocytosis (<4,500).
    4. Analysis/nursing diagnosis:
      1. Altered nutrition, less than body requirements, related to elevated basal metabolic rate.
      2. Risk for injury related to exophthalmos and tremors.
      3. Activity intolerance related to fatigue from overactivity.
      4. Fatigue related to overactivity.
      5. Anxiety related to tachycardia.
      6. Sleep pattern disturbance related to excessive amounts of circulating thyroid hormone.
    5. Nursing care plan/implementation:
      1. Goal: protect from stress: private room, restrict visitors, quiet environment.
      2. Goal: promote physical and emotional equilibrium.
        1. Environment: quiet, cool, well ventilated.
        2. Eye care:
          1. Sunglasses to protect from photophobia, dust, wind.
          2. pillImageProtective drops (methylcellulose) to soothe exposed cornea.
        3. foodImageDiet:
          1. High: calorie, protein, vitamin B.
          2. 6 meals/day, as needed.
          3. Weigh daily.
          4. Avoid stimulants (coffee, tea, colas, tobacco).
      3. Goal: prevent complications.
        1. pillImageMedications as ordered:
          1. Propylthiouracil to block thyroid synthesis; hyperthyroidism returns when therapy is stopped.
          2. Methimazole (Tapazole) to inhibit synthesis of thyroid hormone.
          3. Iodine preparations: used in combination with other medications when hyperthyroidism not well controlled; saturated solution of potassium iodide (SSKI) or Lugol's solution; more palatable if diluted with water, milk, or juice; give through a straw to prevent staining teeth. Takes 2 to 4 weeks before results are evident.
          4. Propranolol (Inderal), atenolol (Tenormin), metoprolol (Lopressor) given to counteract the increased metabolic effect of thyroid hormones, but do not alter their levels. Relieve the symptoms of tachycardia, tremors, and anxiety.
        2. Monitor for thyroid storm (crisis)—medical emergency: acute episode of thyroid overactivity caused when increased amounts of thyroid hormone are released into the bloodstream and metabolism is markedly increased.
          1. Risk factors for thyroid storm: client with uncontrolled hyperthyroidism (usually Graves' disease) who undergoes severe sudden stress, such as:
            1. Infection.
            2. Surgery.
            3. Beginning labor to give birth.
            4. Taking inadequate antithyroid medications before thyroidectomy.
          2. Assessment:
            1. Subjective data—thyroid storm:
              1. Apprehension.
              2. Restlessness.
            2. Objective data—thyroid storm:
              1. Vital signs: elevated temperature (106°F), hypotension, extreme tachycardia.
              2. Marked respiratory distress, pulmonary edema.
              3. Weakness and delirium.
              4. If untreated, client could die of heart failure.
          3. pillImageMedications—thyroid storm:
            1. Propylthiouracil or methimazole (Tapazole) to decrease synthesis of thyroid hormone.
            2. Sodium iodide IV; Lugol's solution orally to facilitate thyroid hormone synthesis.
            3. Propranolol (Inderal) to slow heart rate.
            4. Aspirin to decrease temperature.
            5. Steroids to combat crisis.
            6. Diuretics, digitalis to treat heart failure.
      4. Goal: health teaching.
        1. Stress-reduction techniques.
        2. Importance of medications, their desired effects and side effects.
        3. Methods to protect eyes from environmental damage.
        4. Signs and symptoms of thyroid storm (see E. 3. b.).
      5. Goal: prepare for additional treatment as needed.
        1. pillImageRadioactive iodine therapy: 131I, a radioactive isotope of iodine to decrease thyroid activity.
          1. 131I dissolved in water and given by mouth.
          2. Hospitalization necessary only when large dose is administered.
          3. Minimal precautions needed for usual dose.
            1. Sleep alone for several nights.
            2. Flush toilet several times after use.
          4. Effectiveness of therapy seen in 2 to 3 weeks; single dose controls 90% of clients.
          5. Monitor for signs of hypothyroidism.
        2. Surgery (see IV. THYROIDECTOMY, following).
    6. Evaluation/outcome criteria:
      1. Complications avoided.
      2. Compliance with medical regimen.
      3. No further weight loss.
      4. Able to obtain adequate sleep.
  4. THYROIDECTOMY: partial removal of thyroid gland (for hyperthyroidism) or total removal (for malignancy of thyroid).
    1. Risk factor: unsuccessful medical treatment of hyperthyroidism.
    2. Analysis/nursing diagnosis:
      1. Risk for injury related to possible trauma to parathyroid gland during surgery.
      2. Ineffective breathing pattern related to neck incision.
      3. Pain related to surgical incision.
      4. Altered nutrition, less than body requirements, related to difficulty in swallowing because of neck incision.
      5. Impaired verbal communication related to possible trauma to nerve during surgery.
      6. Risk for altered body temperature related to thyroid storm.
    3. Nursing care plan/implementation: Prepare for surgery (see I. THE PREOPERATIVE PREPARATION, The Perioperative Experience). Postoperative:
      1. Goal: promote physical and emotional equilibrium.
        1. infoImagePosition: semi-Fowler's to reduce edema.
        2. Immobilize head with pillows/sandbags.
        3. Support head during position changes to avoid stress on sutures, prevent flexion or hyperextension of neck.
      2. pillImageGoal: prevent complications of hypocalcemia and tetany, due to accidental trauma to parathyroid gland during surgery; signs of tetany indicate necessity of calcium gluconate IV.
        1. Check Chvostek's sign—tapping face in front of ear produces spasm of facial muscles.
        2. Check Trousseau's sign—compression of upper arm (usually with BP cuff) elicits carpal (wrist) spasm.
        3. Monitor for respiratory distress (due to laryngeal nerve injury, edema, bleeding); keep tracheostomy set/suction equipment at bedside.
        4. Monitor for elevated temperature, indicative of thyroid storm (see Objective Assessment Data for Thyroid Storm, Physiological Integrity).
        5. Monitor vital signs, check dressing and beneath head, shoulders for bleeding q1h and prn for 24 hours; hemorrhage is possible complication; if swallowing is difficult, loosen dressing. If client still complains of tightness when dressing is loosened, look for further signs of hemorrhage.
        6. Check voice postoperatively as soon as responsive after anesthesia and every hour (assess for possible laryngeal nerve damage ); crowing voice sound indicates laryngeal nerves on both sides have been injured; respiratory distress possible from swelling.
          1. Avoid unnecessary talking to lessen hoarseness.
          2. Provide alternative means of communication.
      3. Goal: promote comfort measures.
        1. pillImageNarcotics as ordered.
        2. Offer iced fluids.
        3. foodImageAmbulation and soft diet, as tolerated.
      4. Goal: health teaching.
        1. How to support neck to prevent pressure on suture line: place both hands behind neck when moving head or coughing.
        2. pillImageSigns of hypothyroidism; needs supplemental thyroid hormone if total thyroidectomy.
        3. Signs and symptoms of hemorrhage and respiratory distress.
        4. Importance of adequate rest and nutritious diet.
        5. Importance of voice rest in early recuperative period.
    4. Evaluation/outcome criteria:
      1. No respiratory distress, hemorrhage, laryngeal damage, tetany.
      2. Preoperative symptoms relieved.
      3. Normal range of neck motion obtained.
      4. States signs and symptoms of possible complications.
  5. HYPOTHYROIDISM (MYXEDEMA): deficiency of circulating thyroid hormone; often a final consequence of Hashimoto's thyroiditisand Graves' disease.
    1. Pathophysiology: atrophy, destruction of gland by endogenous antibodies or inadequate pituitary thyrotropin production → insidious slowing of body processes, personality changes, and generalized, interstitial nonpitting (mucinous) edema—myxedema; pronounced involvement in systems with high protein turnover (e.g., cardiac, GI, reproductive, hematopoietic).
    2. Risk factors:
      1. Total thyroidectomy; inadequate replacement therapy.
      2. Inherited autosomal recessive gene coding for disorder.
      3. Hypophyseal failure.
      4. Dietary iodine deficiencies.
      5. Irradiation of thyroid gland.
      6. Overtreatment of hyperthyroidism.
      7. Chronic lymphocytic thyroiditis.
      8. Postpartum thyroiditis.
      9. Viral thyroiditis.
      10. Medications, such as amiodarone HCl (Cordarone), used to treat abnormal heart rhythms.
    3. Assessment:
      1. Subjective data:
        1. Weakness, fatigue, lethargy.
        2. Headache.
        3. Slow memory, psychotic behavior.
        4. Loss of interest in sexual activity.
      2. Objective data:
        1. Depressed basal metabolic rate (BMR).
        2. Cardiomegaly, bradycardia, hypotension, anemia.
        3. Menorrhagia, amenorrhea, infertility.
        4. Dry skin, brittle nails, coarse hair, hair loss.
        5. Slow speech, hoarseness, thickened tongue.
        6. Weight gain: edema, generalized interstitial; peripheral nonpitting; periorbital puffiness.
        7. Intolerance to cold.
        8. Hypersensitive to narcotics and barbiturates.
        9. Laboratory data:
          1. Elevated: thyroid-releasing hormone (TRH), thyroid-stimulating hormone (TSH), cholesterol (>220 mg/dL), lipids (>850 mg/dL), protein (>8 gm/dL).
          2. Normal-low: serum thyroxine (T4), serum triiodothyronine (T3).
          3. Decreased: radioactive iodine uptake (RAIU).
    4. Analysis/nursing diagnosis:
      1. Risk for injury related to hypersensitivity to drugs.
      2. Altered nutrition, more than body requirements, related to decreased BMR.
      3. Activity intolerance related to fatigue.
      4. Constipation related to decreased peristalsis.
      5. Decreased cardiac output related to hypotension and bradycardia.
      6. Risk for impaired skin integrity related to dry skin and edema.
      7. Social isolation related to lethargy.
    5. Nursing care plan/implementation:
      1. Goal: provide for comfort and safety.
        1. Monitor for infection or trauma; may precipitate myxedema coma, which is manifested by: unresponsiveness, bradycardia, hypoventilation, hypothermia, and hypotension.
        2. Provide warmth; prevent heat loss and vascular collapse.
        3. pillImageAdminister thyroid medications as ordered: levothyroxine (Synthroid)—most common drug used; liothyronine sodium (Cytomel); dosage adjusted according to symptoms.
      2. Goal: health teaching.
        1. Diet: low calorie, high protein.
        2. foodImageSigns and symptoms of hypothyroidism and hyperthyroidism.
        3. Lifelong medications, dosage, desired effects and side effects.
        4. Medication dosage adjustment: take one third to one half the usual dose of narcotics and barbiturates.
        5. Stress-management techniques.
        6. Exercise program.
    6. Evaluation/outcome criteria:
      1. No complications noted. Most common complications: atherosclerotic coronary heart disease, acute organic psychosis, and myxedema coma.
      2. Dietary instructions followed.
      3. Medication regimen followed.
      4. Thyroid hormone balance obtained and maintained.
  6. CUSHING'S DISEASE: an endogenous overproduction of adrenocorticotropic hormone (ACTH) that can be caused by pituitary-dependent adenomas. Cushing's syndrome: condition marked by chronic excessive circulating cortisol with or without pituitary involvement. One of the most common causes of Cushing's syndrome is the administration of cortisone-like medications for treatment of a variety of conditions.
    1. Pathophysiology:
      1. Excess glucocorticoid production, leading to:
        1. Increased gluconeogenesis → raised serum glucose levels → glucose in urine, increased fat deposits in face and trunk.
        2. Decreased amino acids → protein deficiencies, muscle wasting, poor antibody response, and lack of collagen.
    2. Risk factors:
      1. Adrenal hyperplasia.
      2. Excessive hypothalamic stimulation.
      3. Tumors: adrenal, hypophyseal, pituitary, bronchogenic, or gallbladder.
      4. Excessive steroid therapy.
    3. Assessment:
      1. Subjective data:
        1. Headache, backache.
        2. Weakness, decreased work capacity.
        3. Mood swings.
      2. Objective data:
        1. Hypertension, weight gain, pitting edema.
        2. Characteristic fat deposits, truncal and cervical obesity ( buffalo hump).
        3. Pendulous abdomen, purple striae, easy bruising.
        4. Moon facies, acne.
        5. Hyperpigmentation.
        6. Impotence.
        7. Virilization in women: hirsutism, breast atrophy, and amenorrhea.
        8. Pathological fractures, reduced height.
        9. Slow wound healing.
        10. Laboratory data:
          1. Urine: elevated 17-ketosteroids (>12 mg/24 hr) and glucose (>120 mg/dL).
          2. Plasma: elevated 17-hydroxycorticosteroids, cortisol (>10 mcg/dL). Cortisol does not decrease during the day as it should.
          3. Serum: elevated—glucose, RBC, WBC counts; diminished—potassium, chlorides, eosinophils, lymphocytes.
        11. X-rays and scans to determine tumors metastasis.
    4. Analysis/nursing diagnosis:
      1. Body image disturbance related to changes in physical appearance.
      2. Activity intolerance related to backache and weakness.
      3. Risk for injury related to infection and bleeding.
      4. Knowledge deficit (learning need) related to management of disease.
      5. Pain related to headache.
    5. Nursing care plan/implementation:
      1. Goal: promote comfort.
        1. Assist with preparation of diagnostic work-up.
        2. Explain procedures.
        3. Protect from trauma.
      2. Goal: prevent complications; monitor for:
        1. Fluid balance—I&O, daily weights.
        2. Glucose metabolism—blood, urine for sugar and acetone.
        3. Hypertension—vital signs.
        4. Infection—skin care, urinary tract; check temperature.
        5. Mood swings—observe behavior.
      3. Goal: health teaching.
        1. foodImageDiet: increased protein, potassium; decreased calories, sodium.
        2. pillImageMedications:
          1. Cytotoxic agents: aminoglutethimide (Cytadren), trilostane (Modrastane), mitotane (Lysodren)—to decrease cortisol production.
          2. Replacement hormones as needed.
        3. Signs and symptoms of progression of disease as noted in assessment.
        4. Preparation for adrenalectomy if medical regimen unsuccessful.
    6. Evaluation/outcome criteria:
      1. Symptoms controlled by medication.
      2. No complications—adrenal steroids within normal limits.
      3. If adrenalectomy necessary, see VIII. ADRENALECTOMY.
  7. PHEOCHROMOCYTOMA: a rare, typically benign neuroendocrine tumor of the adrenal medulla. Appears to have a familial basis; common in middle age—rare after 60 years.
    1. Pathophysiology: catecholamine-secreting tumor → increased epinephrine and norepinephrine (paroxysm) → hypertensive retinopathy and nephropathy, myocarditis → cerebral hemorrhage and cardiac failure.
    2. Risk factors for paroxysm:
      1. Voiding.
      2. Smoking.
      3. Drugs (i.e., histamine, anesthesia, atropine, steroids, fentanyl).
      4. Bending, straining, exercising (displacing abdominal organs) → increased abdominal pressure.
    3. Assessment:
      1. Subjective data:
        1. Apprehension.
        2. Pounding headache.
        3. Nausea.
        4. Pain with vomiting.
        5. Visual disturbances.
        6. Palpitations.
        7. Heat intolerance.
      2. Objective data:
        1. Hypertension: rapid onset, abrupt cessation; postural hypotension.
        2. Profuse diaphoresis with acute attack.
        3. Pulse: rapid, dysrhythmia.
        4. Pupils: dilated.
        5. Extremities: cold, tremors.
        6. Laboratory data:
          1. Hyperglycemia, glycosuria.
          2. ↑ Urinary catecholamines: single-voided, 2-to 4-hour specimen and 24-hour urine, greater than 14 mg/100 mL.
          3. Direct assay of catecholamines—epinephrine greater than 0.2 mg/L; norepinephrine 0.5 mg/L.
          4. ↑ BMR.
        7. X-ray, CT, and MRI—used to localize tumor before surgery.
    4. Analysis/nursing diagnosis:
      1. Anxiety related to excessive physiological stimulation of sympathetic nervous system.
      2. Fluid volume deficit related to excessive gastric losses, hypermetabolic state, diaphoresis.
      3. Risk for decreased cardiac output related to excessive secretion of catecholamines as evidenced by hypertension.
      4. Risk for injury related to excessive release of epinephrine and norepinephrine.
      5. Altered nutrition, greater than body requirements, related to elevated glucose.
    5. Nursing care plan/implementation:
      1. Goal: prevent paroxysmal hypertension.
        1. Rest: reduce stress, ↓ environmental stimulation.
        2. pillImageGive sedatives, alpha-adrenergic blocker (phenoxybenzamine) for hypertension and antidysrhythmics as ordered.
        3. foodImageDiet: high vitamin, high calorie, mineral, calcium; restrict caffeine.
        4. Monitor vital signs (especially BP in sitting and supine positions).
      2. Goal: prepare for surgical removal of tumor (see VIII. ADRENALECTOMY, following).
    6. Evaluation/outcome criteria:
      1. No paroxysmal hypertension.
      2. See VIII. ADRENALECTOMY.
  8. ADRENALECTOMY: surgical removal of adrenal glands because of tumors or uncontrolled overactivity; also bilateral adrenalectomy may be performed to control metastatic breast or prostate cancer.
    1. Risk factors:
      1. Pheochromocytoma.
      2. Adrenal hyperplasia.
      3. Cushing's syndrome.
      4. Metastasis of prostate or breast cancer.
      5. Adrenal cortex or medulla tumors.
    2. Assessment:
      1. Objective data: validated evidence of:
        1. Benign lesion (unilateral adrenalectomy) or malignant tumor (bilateral adrenalectomy).
        2. Adrenal hyperfunction that cannot be managed medically.
        3. Bilateral excision for metastasis of breast and sometimes metastasis of prostate cancer.
    3. Analysis/nursing diagnosis:
      1. Knowledge deficit (learning need) related to planned surgery.
      2. Risk for physical injury related to hormone imbalance.
      3. Risk for decreased cardiac output related to possible hypotensive state resulting from surgery.
      4. Risk for infection related to decreased normal resistance.
      5. Altered health maintenance related to need for self-administration of steroid medications, orally or by injection.
    4. Nursing care plan/implementation:
      1. Goal: preoperative: reduce risk of postoperative complications.
        1. pillImagePrescribed steroid therapy, given 1 week before surgery, is gradually decreased; will be given again postoperatively.
        2. Antihypertensive drugs are discontinued because surgery may result in severe hypotension.
        3. pillImageSedation as ordered.
        4. General preoperative measures (see I. PREOPERATIVE PREPARATION, The Perioperative Experience).
      2. Goal: postoperative: promote hormonal balance.
        1. pillImageAdminister hydrocortisone parenteral therapy as ordered; rate indicated by fluid and electrolyte balance, blood sugar, and blood pressure.
        2. Monitor for signs of addisonian (adrenal) crisis(see IX. ADDISON'S DISEASE, Physiological Integrity).
      3. Goal: prevent postoperative complications.
        1. pillImageMonitor vital signs until stability is regained; if on vasopressor drugs such as metaraminol (Aramine):
          1. Maintain flow rate as ordered.
          2. Monitor BP q5–15 min, notify physician of significant elevations in BP (dose needs to be decreased) or drop in BP (dose needs to be increased). Note: readings that are normotensive for some may be hypotensive for clients who have been hypertensive.
        2. NPO—attach nasogastric tubeto intermittent suction; abdominal distention is common side effect of this surgery.
        3. Respiratory care:
          1. Turn, cough, and deep breathe.
          2. Splint flank incision when coughing.
          3. pillImageAdminister narcotics to reduce pain and allow client to cough; flank incision is close to diaphragm, making coughing very painful.
          4. Auscultate breath sounds q2h; decreased or absent sounds could indicate pneumothorax.
          5. Sudden chest pain and dyspnea should be reported immediately (spontaneous pneumothorax).
        4. infoImagePosition: flat or semi-Fowler's.
        5. Mouth care.
        6. Monitor dressings for bleeding; reinforce prn.
        7. Ambulation, as ordered.
          1. Check BP q15 min when ambulation is first attempted.
          2. Place elastic stockings on lower extremities to enhance stability of vascular system.
        8. foodImageDiet—once NG tube removed, diet as tolerated.
      4. Goal: health teaching.
        1. Signs and symptoms of adrenal crisis:
          1. Pulse: rapid, weak, or thready.
          2. Temperature: elevated.
          3. Severe weakness and hypotension.
          4. Headache.
          5. Convulsions, coma.
        2. Importance of maintaining steroid therapy schedule to ensure therapeutic serum level.
        3. Weigh daily.
        4. Monitor blood glucose levels daily.
        5. Report undesirable side effects of steroid therapy or adrenal crisis to physician.
        6. Avoid persons with infections, due to decreased resistance.
        7. Daily schedule: include adequate rest, moderate exercise, good nutrition.
    5. Evaluation/outcome criteria:
      1. Adrenal crisis avoided.
        1. Vital signs within normal limits.
        2. No neurological deficits noted.
      2. Healing progresses: no signs of infection or wound complications.
      3. Adjusts to alterations in physical status.
        1. Complies with medication regimen.
        2. Avoids infections.
        3. Incorporates good nutrition, periods of rest and activity into daily schedule.
  9. ADDISON'S DISEASE: chronic primary adrenal corticotropic insufficiency. A hormonal (endocrine) disorder involving destruction of the adrenal glands, which then are unable to produce sufficient adrenal hormones (cortisol) necessary for the normal body functions.
    1. Pathophysiology:
      1. Atrophy of adrenal gland is most common cause of adrenal insufficiency; manifested by decreased adrenal cortical secretions.
        1. Deficiency in mineralocorticoid secretion ( aldosterone ) → increased sodium excretion → dehydration → hypotension → decreased cardiac output and resulting decrease in heart size.
        2. Deficiency in glucocorticoid secretion ( cortisol ) → decrease in gluconeogenesis → hypoglycemia and liver glycogen deficiency, emotional disturbances, diminished resistance to stress. Cortisol deficiency → failure to inhibit anterior pituitary secretion of ACTH and melanocyte-stimulating hormone → increased levels of ACTH and hyperpigmentation.
        3. Deficiency in androgen hormone → less axillary and pubic hair in women (testes supply adequate sex hormone in men, so no symptoms are produced).
    2. Risk factors:
      1. Autoimmune processes.
      2. Infection.
      3. Malignancy.
      4. Vascular obstruction.
      5. Bleeding.
      6. Environmental hazards.
      7. Congenital defects.
      8. Bilateral adrenalectomy.
      9. Tuberculosis.
    3. Assessment:
      1. Subjective data:
        1. Muscle weakness, fatigue, lethargy.
        2. Dizziness, fainting.
        3. Nausea, food idiosyncrasies, anorexia.
        4. Abdominal pain/cramps.
      2. Objective data:
        1. Vital signs: decreased BP, orthostatic hypotension, widened pulse pressure.
        2. Pulse—increased, collapsing, irregular.
        3. Temperature—subnormal.
        4. Vomiting, diarrhea, and weight loss.
        5. Tremors.
        6. Skin: poor turgor, excessive pigmentation ( bronze tone ).
        7. Laboratory data:
          1. Blood:
            1. Decreased: sodium (<135 mEq/L); glucose (<60 mg/dL), chloride (<98 mEq/L), bicarbonate (<23 mEq/L).
            2. Increased: hematocrit, potassium (>5 mEq/L).
          2. Urine: decreased (or absent) 17-ketosteroids, 17-hydroxycorticosteroids (<5 mg/24 hr).
        8. Diagnostic tests:
          1. CT scan, MRI.
          2. ACTH stimulation test (cortisol levels are measured before and after administration of synthetic ACTH).
    4. Analysis/nursing diagnosis:
      1. Fluid volume deficit related to decreased sodium.
      2. Altered renal tissue perfusion related to hypotension.
      3. Decreased cardiac output related to aldosterone deficiency.
      4. Risk for infection related to cortisol deficiency.
      5. Activity intolerance related to muscle weakness and fatigue.
      6. Altered nutrition, less than body requirements, related to nausea, anorexia, and vomiting.
    5. Nursing care plan/implementation:
      1. Goal: decrease stress.
        1. Environment: quiet, nondemanding schedule.
        2. Anticipate events for which extra resources will be necessary.
      2. Goal: promote adequate nutrition.
        1. foodImageDiet: acute phase—high sodium, low potassium; nonacute phase—increase carbohydrates and protein.
        2. Fluids: force, to balance fluid losses; monitor I&O, daily weights.
        3. pillImageAdminister lifelong exogenous replacement therapy as ordered:
          1. Glucocorticoids—prednisone, hydrocortisone.
          2. Mineralocorticoids—fludrocortisone (Florinef).
      3. Goal: health teaching.
        1. pillImageTake medications with food or milk.
        2. May need antacid therapy to prevent GI disturbances.
        3. Side effects of steroid therapy.
        4. Avoid stress; may need adjustment in medication dosage when stress is increased.
        5. Signs and symptoms of addisonian (adrenal) crisis: very serious condition characterized by severe hypotension, shock, coma, and vasomotor collapse related to strenuous activity, infection, stress, omission of prescribed medications. If untreated, could quickly lead to death.
      4. Goal: prevent serious complications if addisonian crisis evident.
        1. pillImageComplete bedrest; avoid stimuli.
        2. High dose of hydrocortisone IV or cortisone IM.
        3. Treat shock—IV saline.
        4. I&O, vital signs q15 min to 1 hour or prn until crisis passes.
    6. Evaluation/outcome criteria:
      1. No complications occur.
      2. Medication regimen followed, is adequate for client's needs.
      3. Adequate nutrition and fluid balance obtained.