NSG210 Hinkle Ch. 45: Assessment and Management of Patients with Endocrine Disorders

Source: Hinkle & Cheever, Brunner & Suddarth’s Medical-Surgical Nursing 15e, Chapter 45, pp. 1445-1486 (textbooks/HINKLE_MS_CH45.pdf, also in textbooks/exam04/). Week 15 reading (regulation and metabolism: thyroid and parathyroid disorders, corticosteroid therapy); Exam 4 content. Numbering note: the syllabus lists “Ch. 46” (16th edition); endocrine disorders is Ch. 45 in the 15th edition (15e Ch. 46 is diabetes). See nsg210-textbook-chapter-crosswalk. Pancreatic islet physiology is in nsg210-hinkle-ch44-biliary-pancreatic; DI and SIADH after neurosurgery are in nsg210-hinkle-ch61-neurologic-dysfunction.

Learning Outcomes

1. Describe the functions of each endocrine gland and its hormones.
2. Differentiate diagnostic studies and clinical manifestations of endocrine disorders.
3. Demonstrate knowledge of management strategies for endocrine disorders.
4. Explain nursing interventions for patients with endocrine disorders.
5. Use the nursing process for the patient with an endocrine disorder.

Key Terms

• Acromegaly: enlargement of peripheral body parts from excess growth hormone (GH) in adults
• Addison disease: chronic adrenocortical insufficiency. Addisonian crisis: acute insufficiency with hypotension, cyanosis, fever, nausea, vomiting, shock
• ACTH: adrenocorticotropic hormone from anterior pituitary
• Calcitonin: thyroid hormone that lowers serum calcium by increasing bone deposition
• Chvostek sign: facial muscle spasm when tapping the facial nerve in front of the ear (latent tetany, hypocalcemia)
• Trousseau sign: carpopedal spasm when BP cuff occludes arm blood flow for 3 minutes (latent tetany)
• Cushing syndrome: excess glucocorticoids: truncal obesity, moon face, acne, abdominal striae, hypertension
• Diabetes insipidus (DI): large volumes of dilute urine from deficient vasopressin
• Euthyroid: normal thyroid hormone production
• Exophthalmos: protruding eyeballs. Goiter: enlarged thyroid. Graves disease: hyperthyroidism with diffuse goiter and exophthalmos
• Glucocorticoids: raise glucose (cortisol). Mineralocorticoids: electrolyte balance (aldosterone)
• Myxedema: severe hypothyroidism (with or without coma)
• Negative feedback: rising hormone level suppresses its own production
• Pheochromocytoma: adrenal medulla tumor
• SIADH: excess ADH despite low serum osmolality
• Thyroid storm: life-threatening untreated hyperthyroidism. Thyrotoxicosis: excess thyroid hormone (endogenous or exogenous)
• T4 (thyroxine): weaker, steady-state; T3 (triiodothyronine): about 5 times more potent, faster
• Vasopressin: antidiuretic hormone (ADH) from posterior pituitary

I. Endocrine Overview and Assessment

• Glands: pituitary, thyroid, parathyroids, adrenals, pancreatic islets, ovaries, testes. Hypothalamus links endocrine, nervous, and immune systems.
• Negative feedback keeps hormone levels constant. Hormone classes: amines/amino acids (epinephrine, thyroid hormones), peptides/proteins (TRH, FSH, GH), steroids (corticosteroids), fatty acid derivatives. Peptides act via cell-surface receptors and cyclic AMP (fast); steroids enter cells and change protein synthesis (hours).
• History: changes in energy, heat or cold tolerance, weight, thirst, urination, bowel function, body proportions, muscle mass, fat distribution, hair, menses, memory, concentration, sleep, mood, vision, joint pain, sexual function.
• Exam: VS, skin, hair, thyroid palpation; facial hair in women, moon face, buffalo hump, exophthalmos, edema, thin skin, truncal obesity, thin extremities, enlarged hands and feet, hypo- or hyperreflexia; nervousness, lethargy.
• Diagnostics: blood hormone levels and autoantibodies; 24-hour urine (catecholamines for pheochromocytoma); stimulation tests (confirm hypofunction); suppression tests (confirm hyperfunction); imaging (MRI, CT, ultrasound, PET, DXA); genetic testing.

II. Pituitary Gland

A. Physiology

• Master gland; controlled by the hypothalamus via the pituitary stalk.
• Anterior: FSH, LH, prolactin, ACTH, TSH, GH (most abundant; growth in children, metabolism in adults; raises glucose; increased by deep sleep, stress, exercise, fasting, hypoglycemia, trauma, shock, sepsis).
• Posterior: stores vasopressin (ADH; water excretion; released with rising osmolality or falling BP) and oxytocin (labor, milk ejection), both made in the hypothalamus.

B. Pathophysiology

• Hypersecretion: ACTH (Cushing) or GH (acromegaly in adults; gigantism in children before growth plates fuse, may reach 7 to 8 feet).
• Hyposecretion: dwarfism; panhypopituitarism (thyroid, adrenal cortex, gonads atrophy). Total destruction leads to weight loss, emaciation, hair loss, impotence, amenorrhea, hypometabolism, hypoglycemia, coma, death if not replaced.
• Posterior lobe: DI most common.

C. Pituitary Tumors

• Almost all benign, slow growing; functional or nonfunctional.
• Eosinophilic: gigantism or acromegaly (enlarged hands, feet, brow, cheekbones, nose, chin, all organs); headaches; visual disturbances from optic nerve pressure (loss of color discrimination, diplopia, field defects).
• Basophilic: Cushing syndrome (masculinization, amenorrhea, truncal obesity, hypertension, osteoporosis, polycythemia).
• Chromophobic (90 percent): usually nonsecreting but destroy pituitary causing hypopituitarism (obesity, somnolence, scanty hair, pasty complexion, headache, loss of libido, visual loss, polyuria, polyphagia, low BMR, subnormal temperature).
• Diagnosis: history, visual acuity and fields, CT, MRI, hormone levels.
• Treatment: transsphenoidal hypophysectomy (usual; treatment of choice for pituitary Cushing disease); stereotactic or conventional radiation; bromocriptine, octreotide, lanreotide (lower GH, shrink tumor). Acromegaly features are not reversed by surgery. After total removal: infertility, menses stop; lifelong corticosteroid and thyroid replacement.

D. Diabetes Insipidus

• Deficient ADH (or kidney unresponsive): huge output of dilute urine and extreme thirst.
• Types: central (head trauma most common; surgery, infection, tumors, vascular disease, idiopathic), nephrogenic (kidney injury, lithium, hypokalemia, hypercalcemia), dipsogenic, gestational.
• Signs: urine output over 250 mL/h; specific gravity 1.001 to 1.005; no glucose or albumin; drinks 2 to 20 L/day, craves cold water. Restricting fluids does NOT reduce output; causes hypernatremia and severe dehydration.
• Fluid deprivation test: withhold fluids 8 to 12 hours or until 3 to 5 percent body weight lost; weigh frequently; urine stays dilute in DI; stop test for tachycardia, excessive weight loss, hypotension.
• Treatment: desmopressin (DDAVP; synthetic vasopressin, oral or intranasal; drug of choice for central DI). Vasopressin causes vasoconstriction, caution in CAD. Chlorpropamide and thiazides for mild DI (hypoglycemia risk). Nephrogenic: thiazides, mild salt depletion, prostaglandin inhibitors (indomethacin, aspirin).
• Nursing: watch for dehydration (decreased cardiac output, brain and kidney perfusion); VS, I&O; teach medication administration with return demonstration; signs of hyponatremia (overreplacement); medical ID bracelet.

E. SIADH

• Failure of negative feedback: cannot excrete dilute urine, water retention, dilutional hyponatremia.
• Causes: bronchogenic lung cancer producing ADH, severe pneumonia, pneumothorax, other lung disorders, other cancers; CNS injury, surgery, tumor, infection; drugs (vincristine, phenothiazines, tricyclics, thiazides), nicotine.
• Treatment: correct cause; fluid restriction; furosemide with fluid restriction; 3 percent hypertonic saline IV for severe hyponatremia.
• Nursing: I&O, daily weight, urine and blood chemistries, neuro status.

III. Thyroid Gland

A. Physiology

• Largest endocrine gland; butterfly shape anterior to trachea; about 30 g; very high blood flow.
• Hormones: T4, T3 (iodine required; carried by TBG, transthyretin, albumin), calcitonin (lowers calcium).
• Regulation: hypothalamic TRH stimulates pituitary TSH, which stimulates T3 and T4; high T3/T4 suppresses TSH (negative feedback). Cold increases TRH.
• Thyroid hormone controls metabolic rate, oxygen consumption, heat production, cholesterol, vascular resistance, growth, brain development.
• Iodine deficiency: low T3/T4 leads to high TSH and goiter.

B. Assessment

• Inspect lower neck; have patient extend neck and swallow (thyroid rises). Palpate from front or behind; isthmus normally the only palpable part. Enlarged gland: auscultate for bruit (increased flow, hyperthyroidism). Soft (Graves), firm (Hashimoto, malignancy), tender (thyroiditis).

C. Thyroid Tests

• Serum TSH: primary screening test; monitors replacement therapy; separates thyroid from pituitary/hypothalamic disorders.
• Free T4: 0.7 to 2.0 ng/dL; correlates with metabolic status; high in hyperthyroidism, low in hypothyroidism; best for monitoring treatment of hyperthyroidism.
• Total T4: 5.4 to 11.5 mcg/dL (text prints the unit as pg/dL, a typo); T3: 260 to 480 pg/dL (T3 may better reflect hyperthyroidism). Affected by illness, oral contraceptives, steroids, carbamazepine, salicylates, androgens.
• T3 resin uptake: 25 to 35 percent; over 35 percent hyperthyroidism, under 25 percent hypothyroidism.
• Thyroid antibodies: positive in Hashimoto (100 percent), Graves (80 percent), chronic autoimmune thyroid disease (90 percent).
• Radioactive iodine uptake: high in hyperthyroidism (up to 90 percent), low in hypothyroidism.
• Fine-needle aspiration biopsy: initial test for thyroid masses.
• Thyroid scan: “hot” (hyperfunctioning) vs “cold” (nonfunctioning; higher malignancy chance, especially single).
• Serum thyroglobulin: detects persistent or recurrent thyroid cancer.
• Nursing: ask about iodine reactions, iodine-containing drugs, contrast, kelp or seaweed; shellfish allergy is to proteins, not iodine. Drugs that alter thyroid tests (Chart 45-2): amiodarone, aspirin, cimetidine, diazepam, estrogens, furosemide, glucocorticoids, heparin, lithium, phenytoin and other anticonvulsants, propranolol.

IV. Hypothyroidism

A. Causes and Types

• Most common adult cause: autoimmune (Hashimoto) thyroiditis. Also after radioiodine, antithyroid drugs, or thyroidectomy for hyperthyroidism; radiation to head and neck; aging atrophy; iodine deficiency or excess; lithium; infiltrative disease.
• Primary (over 95 percent; thyroid itself), central (pituitary = secondary; hypothalamus = tertiary), neonatal (congenital: intellectual disability and stunted growth).
• Myxedema: mucopolysaccharide accumulation; term reserved for severe hypothyroidism.

B. Manifestations

• Fatigue, lethargy, weight gain without increased intake, cold intolerance, dry skin, deep voice, bradycardia, ECG conduction changes, menstrual changes (menorrhagia).
• Severe: subnormal temperature and pulse; thick skin; thin hair, loss of lateral eyebrows; masklike face; periorbital edema; enlarged tongue; slow speech; dulled mentation, apathy; constipation; deafness; dementia-like changes; sleep apnea, pleural and pericardial effusion, respiratory muscle weakness; elevated cholesterol, atherosclerosis, CAD, poor LV function.
• Very sensitive to sedatives, opioids, anesthetics. Unrecognized hypothyroidism in surgery: hypotension, heart failure, altered mental status.

C. Myxedema Coma

• Rare decompensated severe hypothyroidism: hypothermia, unconsciousness. Triggers: infection, illness, sedatives, opioids, missed replacement doses, cold; most often older women in winter.
• Progression: depression, lethargy, somnolence, stupor; respiratory depression, alveolar hypoventilation, CO2 retention, narcosis, coma; hyponatremia, hypoglycemia, hypotension, bradycardia, hypothermia, shock. Mortality about 40 percent even with treatment.

D. Medical Management

• Levothyroxine (synthetic T4): drug of choice; usual range 75 to 150 mcg/day; start low and titrate by TSH; older adults often need about 50 mcg/day.
• Cardiac caution: long-standing hypothyroidism with CAD; replacement raises oxygen demand and catecholamine effects, may cause angina, ACS, arrhythmias. If angina or arrhythmia occurs, stop thyroid hormone immediately; resume cautiously at a lower dose.
• Drug interactions: thyroid hormone increases warfarin effect and cardiovascular effects of adrenergic drugs; insulin and oral hypoglycemic doses may need adjustment; estrogen may require higher thyroid dose; calcium, iron, magnesium, zinc reduce absorption.
• Hypnotics and sedatives: prolonged somnolence, narcosis, fatal respiratory depression; use one half to one third the usual dose.
• Myxedema coma support: ABGs, assisted ventilation, pulse oximetry; fluids cautiously (water intoxication); passive rewarming with blankets, NOT active external heat (heating pads), which raises oxygen demand and causes hypotension.

E. Nursing Management (Chart 45-4)

• Respiratory: rate, depth, SpO2, ABGs; deep breathing, incentive spirometry; verify any hypnotic or sedative order; airway and ventilator support.
• Cardiac: HR, rhythm, BP; ECG for arrhythmias after starting replacement; watch cholesterol and angina.
• Temperature: extra clothing or blankets; avoid external heat sources; protect from cold and drafts; report temperature drops (myxedema coma).
• Cognition: orient, stimulate; reassure family cognitive changes are from the disease and improve with treatment.
• Activity: space activities, assist when fatigued.
• Constipation: fluids, fiber, mobility; laxatives and enemas sparingly.
• Teaching: lifelong daily medication even after symptoms improve; take first thing in the morning with a full glass of water on an empty stomach; signs of over- and underdose (hyperthyroid vs hypothyroid symptoms); when to seek care; diet for weight loss and bowel function; periodic TSH; avoid extreme cold and infection; menstrual changes and pregnancy potential.
• Older adults: subtle or atypical symptoms (fatigue, confusion, depression, apathy, weight loss) mistaken for aging; constipation in one fourth; start low, go slow (angina, heart failure, tachyarrhythmias, confusion and agitation if metabolism raised too fast); symptoms resolve in 3 to 12 weeks but therapy is lifelong; check TSH periodically.

V. Hyperthyroidism

A. Causes and Graves Disease

• Most common causes: Graves disease, toxic multinodular goiter, toxic adenoma; also thyroiditis and excessive thyroid hormone intake.
• Graves: autoimmune, immunoglobulins stimulate the thyroid; women 8 times more than men; onset 20s to 40s; may follow emotional shock, stress, infection.

B. Manifestations

• Anxious, restless, irritable, fine hand tremor, tachycardia, palpitations, heat intolerance, sweating, increased appetite with weight loss, diarrhea, thin skin, fine hair, oligomenorrhea, muscle wasting, insomnia, emotional lability.
• Graves: exophthalmos, reduced blinking, lid retraction (eye changes may not reverse); pretibial myxedema.
• Cardiac: sinus tachycardia, arrhythmias, widened pulse pressure, decreased cardiac output; myocardial hypertrophy and heart failure if untreated.
• Course may remit or progress to emaciation, delirium, heart failure.
• Excess replacement hormone can cause hyperthyroid symptoms and premature osteoporosis.
• Diagnosis: enlarged, soft, possibly pulsating gland with thrill and bruit; low TSH, high free T4, increased radioactive iodine uptake.

C. Medical Management

• Radioactive iodine (I-131): most common treatment for Graves and treatment of choice; single dose effective in 80 to 90 percent; destroys thyroid cells over weeks; eventual hypothyroidism expected. Contraindicated in pregnancy (pregnancy test 48 hours before; avoid conceiving at least 6 months after); no breastfeeding for 6 weeks before. Initial release of hormone can worsen symptoms: watch for thyroid storm; beta-blockers. Free T4 checked at 3 to 6 weeks, then every 1 to 2 months; TSH every 6 to 12 months for life once euthyroid. Radiation precautions per dose: avoid sexual contact, sharing a bed, close contact with children and pregnant women, sharing utensils and cups.
• Antithyroid drugs (thionamides): methimazole and propylthiouracil (PTU) block hormone synthesis and T4 to T3 conversion. Baseline CBC with differential and liver profile. Take in morning on empty stomach 30 minutes before eating. Symptom relief takes weeks; taper over months. Watch for fever, rash, urticaria, agranulocytosis, thrombocytopenia: with sore throat, fever, or mouth ulcers stop drug and call provider. PTU in first trimester (methimazole teratogenic), then switch to methimazole (PTU hepatotoxic). Stopping early usually causes relapse within 6 months.
• Table 45-1: PTU (rash, nausea, vomiting, agranulocytosis, SLE; watch for hypothyroidism); methimazole (more toxic than PTU per table); sodium iodide (given 1 hour after PTU or methimazole); potassium iodide and SSKI (suppress hormone release; mix with juice or milk, sip through straw to prevent tooth staining; stop for rash; watch for iodism); beta-blockers (hold for bradycardia or low cardiac output; caution in heart failure).
• Preop adjunct: SSKI 5 drops every 6 hours; PTU 200 mg every 6 hours; propranolol 60 to 80 mg every 6 hours.
• Iodine toxicity: brown-stained mucous membranes, burning mouth and esophagus, laryngeal edema, shock; stop drug immediately.
• Relapse common (Graves remission 12 to 18 months, often recurs within 12 months); all three treatments can cause relapse or permanent hypothyroidism.
• Surgery: for pregnant women allergic to antithyroid drugs, large goiters, obstructive symptoms, need for rapid control, cannot take drugs; done 4 to 6 weeks after euthyroid; subtotal thyroidectomy removes about five sixths; stop aspirin weeks before.
• Older adults: atypical (anorexia, weight loss, isolated atrial fibrillation, no eye signs), new or worse heart failure or angina; check TSH with unexplained decline; toxic nodular goiter most common cause; radioiodine usually recommended; avoid long-term PTU; beta-blockers with extreme caution.

D. Thyroid Storm (Chart 45-6)

• Severe abrupt hyperthyroidism; almost always fatal if untreated.
• Signs: fever over 38.5 C (101.3 F); tachycardia over 130; exaggerated hyperthyroid symptoms with GI (weight loss, diarrhea, abdominal pain) or cardiovascular (edema, chest pain, dyspnea, palpitations) disturbance; altered mental state (delirium, psychosis, somnolence, coma).
• Triggers: injury, infection, thyroid or other surgery, tooth extraction, insulin reaction, DKA, pregnancy, digitalis toxicity, abrupt stop of antithyroid drugs, emotional stress, vigorous thyroid palpation.
• Management: cooling (hypothermia blanket, ice packs, cool room), acetaminophen (NOT salicylates, which free thyroid hormone from binding proteins); humidified oxygen; IV fluids with dextrose (restore glycogen); PTU or methimazole; hydrocortisone (shock, adrenal insufficiency); iodine to reduce T4 release; propranolol (with digitalis) for cardiac symptoms; cardiac monitor, electrolytes, strict I&O.

E. Nursing Process: Hyperthyroidism

• Diagnoses: risk for impaired cardiac function; impaired nutrition; difficulty coping; situational low self-esteem; risk for impaired thermoregulation. Complications: thyroid storm, hypothyroidism.
• Cardiac: VS, HR and rhythm, temperature; palpitations (“heart racing”); heart failure signs (dyspnea, JVD, crackles, edema).
• Nutrition: small frequent high-calorie, high-protein meals; replace fluid from diarrhea and sweating; avoid highly seasoned foods, coffee, tea, cola, alcohol; quiet meals; record weight and intake.
• Coping: reassure that emotional reactions are from the disease and improve with treatment; calm unhurried approach; quiet uncluttered room; balance activity and rest; repeat education (short attention span).
• Self-esteem and eyes: eye drops or ointment for exposed cornea; stop smoking; explain large appetite to family.
• Temperature: cool room, change linens, cool baths and fluids.
• Long-term: risk of hypothyroidism after any treatment; patients may stop replacement once they feel well; teach lifelong therapy; avoid stress that can trigger storm.

VI. Thyroid Tumors and Thyroid Surgery

A. Goiter

• Toxic (with hyperthyroidism) vs nontoxic (euthyroid).
• Endemic (iodine-deficient) simple or colloid goiter: compensatory hypertrophy from TSH; goitrogens, excess iodine, lithium; usually no symptoms except swelling, possible tracheal compression; iodine supplements (SSKI); iodized salt is the most effective prevention.
• Nodular goiter: hyperplasia; may cause pressure symptoms, become malignant, or be hyperthyroid; may need surgery.

B. Thyroid Cancer

• 90 percent of endocrine cancers; incidence tripled in 30 years; women 3 times men; more often under 50.
• Risk: childhood head, neck, or chest radiation (5 to 40 years later); smoking, low activity, unhealthy diet, stress.
• Single, hard, fixed nodule or cervical lymphadenopathy suggests malignancy. Ultrasound-guided fine-needle biopsy is the standard.
• Types: well-differentiated (papillary, most common and least aggressive, best prognosis; follicular, more aggressive).
• Treatment: total or near-total thyroidectomy; neck dissection if nodes involved; spare parathyroids; radioactive iodine ablation afterward and for metastases (side effects: neck soreness, nausea, swollen tender salivary glands, dry mouth, taste change); thyroid hormone to keep TSH suppressed or lifelong replacement; external radiation (mucositis, dry mouth, dysphagia, skin redness).
• Follow-up: TSH, free T4, thyroglobulin, neck ultrasound; calcium and phosphorus; watch for nodules, hoarseness, dysphagia, dyspnea.

C. Thyroidectomy Nursing Care

• Preop: reduce stress (avoid thyroid storm); high-carbohydrate, high-protein, high-calorie diet; thiamine and vitamin C; avoid caffeine and stimulants; good rest; teach supporting the neck with hands behind the head (elbows raised) when moving.
• Postop priorities: airway (glottic edema, hematoma, recurrent laryngeal nerve injury); pulse and BP for bleeding; check sides and back of the neck and dressing for blood; report pressure or fullness at incision (hematoma); tracheostomy set at bedside; call surgeon at first sign of respiratory distress (hematoma needs evacuation).
• Semi-Fowler with head supported by pillows; support head when moving; avoid tension on sutures; overbed table so patient need not turn head; humidifier.
• IV fluids; water once nausea subsides; cold fluids and ice easier; soft diet often preferred.
• Voice: limit talking; note any voice change (recurrent laryngeal nerve injury). Quality and Safety Alert: difficulty speaking may mean edema, nerve damage, or hemorrhage; report immediately.
• Sutures removed 5 to 7 days if nonabsorbable; often discharged same day.
• Hypocalcemia from parathyroid injury or removal: tetany (nerve hyperirritability, hand and foot spasms, muscle twitching); laryngospasm can obstruct airway; treat with IV calcium gluconate; usually temporary unless all parathyroid tissue removed.

VII. Parathyroid Glands

A. Physiology

• Usually four glands behind the thyroid; parathormone (PTH) raises serum calcium (kidney, intestine, bone absorption; helped by vitamin D) and lowers phosphorus; ionized calcium controls PTH by negative feedback.

B. Hyperparathyroidism

• Primary: women 2 to 4 times men; peak 60 to 70; half asymptomatic. Secondary: chronic kidney failure (phosphorus retention, “renal rickets”).
• Signs (hypercalcemia): apathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension, arrhythmias, irritability to psychosis.
• Nephrolithiasis (15 to 20 percent of new cases), kidney damage; bone demineralization, giant cell bone tumors, skeletal pain, pathologic fractures, deformities, shortened stature; peptic ulcer and pancreatitis.
• Diagnosis: persistently elevated serum calcium and PTH; x-ray, bone scan; ultrasound, MRI, thallium scan, biopsy.
• Surgery: parathyroidectomy (minimally invasive, often outpatient). Indications for asymptomatic patients: under 50; unable to follow up; calcium more than 1 mg/dL above normal; GFR under 60; urine calcium over 400 mg/day; T score under -2.5 or prior fracture; kidney stones or nephrocalcinosis.
• Hydration: 2000 mL or more fluid daily to prevent stones; report abdominal pain, hematuria; avoid thiazides (raise calcium); avoid dehydration (vomiting, diarrhea) because of hypercalcemic crisis risk.
• Mobility: walking reduces bone calcium loss; bed rest increases calcium excretion and stones. Oral phosphates short term only.
• Diet: avoid restricted or excess calcium; antacids and protein feedings with peptic ulcer; prune juice, stool softeners, activity for constipation.
• Postop: like thyroidectomy; watch for tetany; transient hypocalcemia (longer with significant bone disease); follow-up calcium levels.

C. Hypercalcemic Crisis

• Calcium over 13 mg/dL: life-threatening neurologic, cardiovascular, kidney symptoms.
• Treatment: rapid IV isotonic saline to urine output 100 to 150 mL/h plus calcitonin; watch for fluid overload; loop diuretic only if edema (not first line unless heart failure or kidney insufficiency); bisphosphonates (etidronate, pamidronate) for sustained decrease; calcitonin with corticosteroids in emergencies; mithramycin, dialysis.

D. Hypoparathyroidism

• Causes: most commonly near-total thyroidectomy; also autoimmune destruction, abnormal development, vitamin D deficiency.
• Low PTH: hypocalcemia and hyperphosphatemia.
• Tetany: latent (numbness, tingling, cramps, stiff hands and feet) and overt (bronchospasm, laryngeal spasm, carpopedal spasm, dysphagia, photophobia, arrhythmias, seizures); anxiety, irritability, depression, delirium; ECG changes, hypotension.
• Positive Chvostek or Trousseau sign suggests latent tetany. Labs: low calcium, high phosphate; dense bones; basal ganglia calcification.
• Goal calcium 9 to 10 mg/dL.
• Acute tetany after thyroidectomy: IV calcium gluconate immediately; sedatives (pentobarbital) if irritability and seizures persist; quiet environment free of noise, drafts, bright lights, sudden movement; tracheostomy or ventilation and bronchodilators if respiratory distress.
• Chronic: calcium, magnesium, calcitriol (preferred) or ergocalciferol; thiazide to reduce urinary calcium loss; diet high in calcium, low in phosphorus (limit milk, milk products, egg yolk, which are also high in phosphorus; avoid spinach, which has oxalate); oral calcium salts; aluminum hydroxide gel or carbonate after meals to bind phosphate.
• Nursing: have calcium gluconate available for emergency IV use; give slowly and cautiously with cardiac disease, arrhythmias, or digitalis (calcium and digitalis potentiate each other: fatal arrhythmias; continuous cardiac monitoring); teach symptoms of hypo- and hypercalcemia.

VIII. Adrenal Glands

A. Physiology

• Medulla: catecholamines (about 90 percent epinephrine): fight-or-flight, raise glucose and metabolic rate.
• Cortex (necessary for life; stress adaptation), regulated by hypothalamic CRH and pituitary ACTH (negative feedback):
  • Glucocorticoids (cortisol): raise glucose; affect nearly all organs. Exogenous high doses suppress ACTH and cause adrenal atrophy; abrupt stop causes adrenal insufficiency.
  • Mineralocorticoids (aldosterone): sodium retention, potassium and hydrogen excretion; driven mainly by angiotensin II (renin) and hyperkalemia, minimally by ACTH.
  • Androgens: excess causes masculinization in women, feminization in men, precocious puberty (adrenogenital syndrome).

B. Pheochromocytoma

• Rare, usually benign catecholamine-secreting tumor; 90 percent in adrenal medulla; causes 0.1 percent of hypertension; usually fatal if untreated, usually cured by surgery; peak 40 to 50; 10 percent bilateral, 10 percent malignant; familial forms (MEN 2: screen family).
• Triad: headache, diaphoresis, palpitations in a hypertensive patient. “Five Hs”: hypertension, headache, hyperhidrosis, hypermetabolism, hyperglycemia. Tremor, flushing, anxiety.
• Paroxysmal attacks (seconds to hours): extreme anxiety, tremor, weakness, headache, vertigo, blurred vision, tinnitus, air hunger, polyuria, nausea, vomiting, diarrhea, abdominal pain, impending doom; BP may exceed 250/150 (arrhythmias, dissecting aneurysm, stroke, acute kidney failure). Orthostatic hypotension in 70 percent untreated.
• Diagnosis: plasma free metanephrines (negative test essentially excludes); 24-hour urine catecholamines, metanephrines, VMA (avoid coffee and tea including decaf, bananas, chocolate, vanilla, aspirin); plasma catecholamines drawn supine after 30 minutes rest with IV placed 30 minutes earlier (avoid caffeine, tobacco, stress, decongestants, bronchodilators, amphetamines). Diagnostic: epinephrine over 400 pg/mL or norepinephrine over 2000 pg/mL. Clonidine suppression test (no suppression in pheochromocytoma). CT, MRI, ultrasound, MIBG scintigraphy.
• During an attack: bed rest with HOB elevated (orthostatic BP drop).
• Preop (10 to 14 days or longer): alpha-blocker first (phenoxybenzamine or doxazosin; orthostasis, nasal stuffiness, fatigue, retrograde ejaculation), increased every 2 to 3 days; high-sodium diet or salt supplements; then beta-blocker (propranolol, metoprolol) cautiously for HR. Targets: BP under 130/80 seated, standing systolic over 90; HR 60-70 seated, 70-80 standing. Calcium channel blockers (nifedipine, nicardipine) as alternative; metyrosine if blockers fail. Keep well hydrated.
• Surgery: adrenalectomy (laparoscopic preferred); hypertensive crisis possible with tumor manipulation. Corticosteroids (IV methylprednisolone then oral prednisone) if bilateral or for days to weeks after unilateral. Postop: hypotension and hypoglycemia from sudden catecholamine withdrawal; ECG, arterial pressure, fluids, electrolytes, glucose. Catecholamines rechecked days after surgery.
• Teaching: follow-up for recurrence; corticosteroid schedule, never skip or stop abruptly; home BP monitoring; 24-hour urine collection.

C. Adrenocortical Insufficiency (Addison Disease)

• Primary: autoimmune in 70 to 90 percent; TB, histoplasmosis; bilateral adrenalectomy; drugs (rifampin, barbiturates, ketoconazole); metastatic cancer. Secondary: sudden stop of exogenous corticosteroids (2 to 4 weeks of daily steroids can suppress the cortex).
• Mineralocorticoid loss: sodium, chloride, water loss, potassium retention, low volume and cardiac output. Glucocorticoid loss: hypoglycemia, weakness, lethargy, anorexia, weight loss, nausea, vomiting. High ACTH: hyperpigmentation of skin and mucous membranes (knuckles, knees, skin folds).
• Labs: low early-morning cortisol with high ACTH (primary); hypoglycemia, hyponatremia, hyperkalemia, leukocytosis.
• Addisonian crisis: severe hypotension, cyanosis, fever, nausea, vomiting, shock, pallor, headache, abdominal pain, diarrhea, confusion, restlessness. Triggers: overexertion, cold, infection, decreased salt intake, surgery, dehydration from test prep.
• Crisis treatment: IV hydrocortisone, then 3 to 4 L normal saline or D5; recumbent with legs elevated; vasopressors if hypotension persists; antibiotics if infection; oral intake when tolerated.
• Lifelong replacement of glucocorticoids (hydrocortisone, cortisone, prednisone) and mineralocorticoid (fludrocortisone); extra doses for stress, surgery, illness, third trimester; extra salt with GI losses or heavy sweating.
• Nursing: orthostatic BP and pulse (systolic drop of 20 mm Hg or more = volume depletion); skin color and turgor; weight; avoid stress, cold, overexertion, infection; foods high in sodium during GI upset and hot weather; take steroids with antacids or meals; steroids correct mood swings.
• Teaching (Chart 45-11): lifelong adherence; dose adjustment for stress; medical alert ID and card; avoid strenuous activity in hot, humid weather; increase fluid and salt with sweating; high-carbohydrate, high-protein diet with adequate sodium; warning signs of crisis; emergency kit with injectable hydrocortisone or dexamethasone and how to use it.

D. Cushing Syndrome

• Most common cause: corticosteroid medications. Also ACTH-producing pituitary tumor (Cushing disease), adrenal hyperplasia, ectopic ACTH (bronchogenic carcinoma). Diurnal cortisol rhythm lost.
• Women 20 to 40 five times more than men.
• Manifestations (Chart 45-12): central obesity, buffalo hump, moon face, thin extremities; thin fragile skin, bruising, striae, acne, poor wound healing; weakness, muscle wasting, osteoporosis, kyphosis, vertebral fractures, aseptic necrosis of femur; sodium and water retention, hypertension, heart failure; hyperglycemia or diabetes; hypokalemia, metabolic alkalosis; infection risk (masked signs); peptic ulcer, pancreatitis; cataracts, glaucoma; sleep disturbance; mood changes, depression, psychosis; virilization in women (hirsutism, breast atrophy, amenorrhea, clitoral enlargement, deep voice); loss of libido; visual changes if pituitary tumor.
• Diagnosis: two of three abnormal: serum cortisol (normal high 6-8 AM, low 4-6 PM; rhythm lost), 24-hour urine cortisol (3 times normal plus one other abnormal test), low-dose overnight dexamethasone suppression (1 or 8 mg at bedtime, 8 AM cortisol; under 5 means normal suppression). False elevations: stress, obesity, depression, anticonvulsants, estrogen, rifampin. Labs: high sodium and glucose, low potassium, low eosinophils.
• Treatment: transsphenoidal hypophysectomy for pituitary cause (treatment of choice) or pituitary radiation; adrenalectomy for unilateral adrenal cause; adrenal enzyme inhibitors (metyrapone, aminoglutethimide, mitotane, ketoconazole) for ectopic ACTH. Postop adrenal insufficiency may appear 12 to 48 hours after surgery: temporary hydrocortisone for months. Steroid-induced: taper to lowest dose; alternate-day therapy. Treat diabetes and peptic ulcer; check glucose and stool for blood.
• Nursing: monitor BP, potassium, weight; low-sodium, high-potassium foods; report edema; protective environment and assistance with ambulation (falls, fractures); high protein, calcium, vitamin D diet, low sodium and calories; avoid exposure to infection (signs masked); meticulous skin care, no adhesive tape, frequent repositioning; low-carbohydrate, low-sodium, high-protein diet for weight and edema; explain mood swings; report psychosis.
• Complications: Addisonian crisis after steroid withdrawal, adrenalectomy, or pituitary tumor removal; hyperglycemia (glucose monitoring, possibly insulin teaching).
• Teaching (Chart 45-13): never stop medication abruptly; medical alert ID; monitor BP, glucose, weight; notify dentist and other providers.

E. Primary Aldosteronism (Conn Syndrome)

• Excess aldosterone (adrenal tumor, ovarian tumor, family history); sodium retention, potassium and hydrogen loss.
• Hypertension is the most prominent, almost universal sign; consider in resistant hypertension or hypertension with hypokalemia. Hypokalemia occurs in less than half: weakness, paralysis, cramps, fatigue, polyuria, polydipsia; hypokalemic alkalosis lowers ionized calcium (tetany, positive Chvostek and Trousseau); glucose intolerance.
• Diagnosis: plasma aldosterone/renin ratio (antihypertensives need not be stopped).
• Treatment: laparoscopic adrenalectomy for unilateral disease; postop steroids, fluids, BP support; lifelong steroids if bilateral; stop spironolactone and potassium after surgery; check potassium weekly for 4 weeks; hypokalemia resolves, hypertension resolves in 35 to 60 percent.
• Medical (bilateral hyperplasia or no surgery): spironolactone first line (monitor potassium and creatinine first 4 to 6 weeks; increases digoxin half-life); eplerenone second line.

IX. Corticosteroid Therapy

• Uses: adrenal insufficiency, inflammation, autoimmune disease, allergy, transplant rejection; rheumatoid arthritis, SLE, asthma, MS; acute crises (status asthmaticus, septic shock). Common agents (Table 45-2): beclomethasone, betamethasone, dexamethasone, hydrocortisone, methylprednisolone, prednisone, prednisolone, triamcinolone.
• Adrenal suppression may persist up to 1 year after a course; stress coverage (IV steroids for surgery) needed during that time.
• Timing: give the daily dose early morning (7 to 8 AM) to mimic natural cortisol peak and minimize cushingoid effects; alternate-day therapy reduces pituitary-adrenal suppression in prolonged therapy.
• Tapering: required to allow adrenal recovery and prevent steroid-induced adrenal insufficiency.
• Eyes: topical eye drops for outer eye infections; long-term use raises intraocular pressure (glaucoma) and causes cataracts.
• Skin: topical creams; absorption greater on scalp, face, genital area and on moist skin (after bathing) or with occlusive dressings; overuse of OTC products risks side effects.
• Table 45-3 side effects and nursing actions:
  • Cardiovascular (hypertension, thrombophlebitis, thromboembolism, atherosclerosis): monitor BP, DVT signs, avoid crossing legs, leg exercises, low-sodium and low-fat diet.
  • Immune (infection, masked signs): assess subtle signs, avoid sick contacts, watch for fungal infection, hand hygiene.
  • Eyes (glaucoma, corneal lesions): yearly eye exams.
  • Musculoskeletal (muscle wasting, poor wound healing, osteoporosis, fractures, aseptic necrosis of femoral head): high protein, vitamin C, calcium, vitamin D; fall prevention; bone density testing.
  • Metabolic (hyperglycemia, steroid withdrawal syndrome): rise slowly (orthostatic hypotension); monitor glucose; take as prescribed, never stop abruptly; medical ID; tell all providers including dentist.
  • Appearance (moon face, weight gain, acne): low-calorie, low-sodium diet; changes are temporary.
  • Fluid and electrolytes: I&O, electrolytes.
• Teaching: adrenal insufficiency and underlying symptoms recur if stopped abruptly; always keep an adequate supply.

High-Yield Numbers

Priority Nursing Actions and Red Flags

• After thyroidectomy: airway first; tracheostomy set at bedside; neck pressure or fullness, bleeding behind the neck, stridor, voice change: call surgeon.
• Tetany (tingling, carpopedal spasm, laryngospasm) after thyroid or parathyroid surgery: IV calcium gluconate; slow with digitalis.
• Thyroid storm: fever over 38.5 C, HR over 130, delirium: cool, acetaminophen (no aspirin), oxygen, PTU or methimazole, iodine, hydrocortisone, beta-blocker.
• Antithyroid drug plus sore throat or fever: stop drug, check CBC (agranulocytosis).
• Hypothyroid patient: watch sedatives and opioids; starting levothyroxine can cause angina; passive rewarming only.
• DI: hourly urine and specific gravity; do not restrict fluids; desmopressin.
• SIADH: fluid restriction; monitor sodium and neuro status.
• Addisonian crisis: IV hydrocortisone and saline, legs elevated; never stop steroids abruptly; stress dosing.
• Pheochromocytoma: alpha-blocker before beta-blocker; HOB up during attacks; postop hypotension and hypoglycemia.
• Cushing or steroid therapy: infection signs masked; fall and fracture prevention; check glucose and potassium.
• Hyperparathyroidism: push fluids, keep mobile, avoid thiazides.

Medications

Related

• nsg210-hinkle-ch44-biliary-pancreatic
• nsg210-hinkle-ch43-hepatic-disorders
• nsg210-hinkle-ch61-neurologic-dysfunction (DI, SIADH, transsphenoidal surgery)
• nsg210-hinkle-ch65-degenerative-neuro (pituitary tumors)
• INDEX