asymptomatic, skeletal disease, renal involvement, GI tract disorders, neurologic abnormalities

Transcription

1 Wk 12. Management of Clients with Parathyroid Disorders and Adrenal glands 2. Parathyroid disorders 1) Hyperparathyroidism Caused by overactivity of one or more of the parathyroid glands Primary, secondary, or tertiary 1) Etiology and Risk Factors Primary: interruption of regulatory relationship between serum calcium and PTH Secondary: hyperplastic gland d/t renal failure, multiple myeloma, carcinoma with bone metastasis 2) Pathophysiology Normal PTH: increase bone resorption proper balance of calcium and phosphorus ions (1) Primary Excessive PTH stimulates transport of calcium into blood Nephrolithiasis: secondary to calcium phosphate kidney stones and deposition of calcium (2) Secondary Chronic renal failure, hyperphosphatemia GFR decreases in CRF, serum phosphorus rise causes decrease in serum calcium level PTH secretion is stimulated 3) Clinical Manifestations asymptomatic, skeletal disease, renal involvement, GI tract disorders, neurologic abnormalities Major complications: dehydration, hypocalcemia, and gastrointestinal problems 4) Diagnosis Lab and x-ray findings Serum calcium levels, depressed serum phosphate levels 5) Medical Management lowering severely elevated calcium levels long-term management of hypercalcemia Serum calcium levels lowered by hydration and calciuria Hydration: N/S infusion Furosemide (Lasix): loop diuretic to promote calciuria after rehydration Plicamycin (Mithracin), gallium nitrate (Ganite), phosphates, calcitonin inhibit bone resorption Plicamycin: chemotherapeutic drug effective in lowering serum calcium levels Gallium nitrate: newer drug, even fewer side effects 1

2 6) Nursing Management Impaired Urinary Elimination Important to resume normal U/O by urine 0.5 ml/kg/hour without development of stones Encourage Fluids: at least 3000 ml of fluid each day 7) Surgical Management Parathyroidectomy Treatment of primary hyperparathyroidism Autotransplantation: after partial parathyroidectomy transplant remaining healthy parathyroid tissue to a safer location such as brachioradial muscle of the forearm Complications: Hypocalcemia potentially life-threatening respiratory distress related either to hemorrhage or to recurrent laryngeal nerve damage 8) Nursing Management Risk for Injury Digitalis: hypercalcemia are hypersensitive to digitalis 2) Hypoparathyroidism deficiency of PTH PTH: primarily regulate calcium balance, hypoparathyroidism hypocalcemia: paresthesia, tetany Irreversible complications: cataracts and basal ganglion, calcifications <Causes> 3 major causes: congenital absence or malfunction of the parathyroid glands autoimmune destruction removal of or injury to one or more parathyroid glands during neck surgery <Pathophysiology> PTH maintains serum calcium levels increasing bone resorption, stimulating renal conversion of vitamin D to its active form <signs and symptoms> neuromuscular irritability increased deep tendon reflexes positive Chvostek s and Trousseau s signs dysphagia <Diagnosis> 2

3 decreased PTH and serum calcium levels, elevated serum phosphorus levels X-rays : increased bone density <Treatment> vitamin D with supplemental calcium dihydrotachysterol if renal function is okay Tetany management Toxic trouble Acute life-threatening tetany: immediate IV calcium, sedatives and anticonvulsants Chronic tetany: vitamin D and possibly oral calcium supplements maintain I.V. line and keep 10% calcium gluconate solution available seizure precautions Keep a tracheostomy tray and an ET tube at bedside b/c laryngospasm from hypocalcemia Monitor for Chvostek s and Trousseau s signs monitor the onset of tetany: minor muscle twitching (in hands), sign of laryngospasm Pts with prolonged QT intervals ventricular arrhythmias, heart block, signs of decreased cardiac output Patient Education signs and symptoms of hypocalcemia and hypercalcemia identify high-calcium, low-phosphorus foods importance of good nail grooming and the need for emollient creams to soften the skin on drug therapy: keep medications away from light 3

4 3. Adrenocortical Disorders Glandular hypofunction and hyperfunction Underactivity deficiency of glucocorticoids, mineralocorticoids, adrenal androgens 1) Adrenal insufficiency Primary: hypofunction in adrenal gland itself Secondary: hypofunction of the pituitaryhypothalamic unit 1-1) Primary adrenal insufficiency Commonly known as Addison s disease idiopathic atrophy or destruction of adrenal glands by autoimmune process or other disease 1) Etiology and Risk Factors rare disorder, incidence and prevalence are unknown autoimmune process : 75% of primary common in AIDS, Tuberculosis 2) Pathophysiology most common cause: autoimmunity, lymphocytic infiltration Gradual destruction chronic adrenal insufficiency deficiency of mineralocorticoids, glucocorticoids 3) Clinical Manifestations usually insidious onset 4) Diagnosis primarily on blood and urine hormonal assays low cortisol production rate and a high plasma ACTH concentration 5) Medical Management (1) Addisonian Crisis acute adrenal insufficiency: under stress without appropriate hormone replacement Stressors: pregnancy, surgery, infection, dehydration, anorexia, fever, emotional upheaval Correct Fluid and Electrolyte Imbalances Rapid rehydration: isotonic solution to correct volume depletion, salt depletion, hypotension oxygen, vasopressors, volume expanders Correct Hypoglycemia IV glucose (5% dextrose [D5] solution IV or IV glucose push bolus) Replace Steroids 4

5 Hydrocortisone 100 mg IV bolus 100 mg IV every 8 hours for 24 hours (2) Addison s Disease Use corticosteroids with caution: glucocorticoid, mineralocorticoid replacement Carefully assess for manifestations of hypercortisolism can result from excessive long-term cortisol therapy 6) Nursing Management (1) Addisonian Crisis Risk for Injury: Addisonian Crisis Monitor for Manifestations of Crisis usually develops over 24 to 48 hours dosage gradually reduced IM or IV every 8 hours on days 1 and 2 of crisis, gradually reduced Control hypoglycemia : glucose infusion as part of rehydration Control hyperkalemia with Kayexalate Observe symptoms of glucocorticoid overdose and overhydration generalized edema from fluid retention, hypertension, flaccid paralysis from hypokalemia psychosis, loss of consciousness usually resolves within 12 hours can tolerate food and fluids by mouth oral steroid replacement Dexamethasone in a prepared syringe in emergency kit with sterile alcohol wipes 7) Self-Care extensive instruction in self-care activities to achieve independence Stable weight, V/S, cortisol levels, decreased fatigue Steroid Replacement written instructions on self-administration of steroids Actions of prescribed hormones (hydrocortisone, fludrocortisone) Importance of taking medications daily, exactly as prescribed Principles of self-administration of oral medications When experiencing stressful situations: emotional upheavals, dental extractions, minor surgery, upper respiratory tract infections general rule: double glucocorticoid dosage for up to 1week, then resume normal dosage Reduce temporary mineralocorticoid dosage by 50% Follow-Up Monitoring semi-annual appointments 5

6 1-2) Secondary adrenal insufficiency Cause: chronic treatment with glucocorticoids for non-endocrine uses Hypopituitarism by the pituitary gland, causes decreased secretion of cortisol and androgens Pituitary tumor or infarction Radiation Suppression of hypothalamic-pituitary secretion of ACTH 2) Adrenocortical hyperfunction Hyperfunction of the adrenal cortex excessive glucocorticoids, mineralocorticoids, androgens hypercortisolism (glucocorticoid excess), primary aldosteronism (aldosterone excess) 2-1) Hypercortisolism Cushing s syndrome, adrenal gland overactivity hypersecretion of glucocorticoids 1) Etiology and Risk Factors Iatrogenic hypercortisolism caused by a cortisolsecreting, adrenal tumor, adrenal hyperplasia Adrenal tumors: 30% of Cushing s syndrome most (85%) are benign - Pituitary hypersecretion, pituitary tumors - Ectopic secretion of ACTH (or ectopic ACTH syndrome) exogenous administration of synthetic glucocorticoids Health maintenance activities educating who are at risk treating hypernatremia, hypokalemia, hyperglycemia, hypertension teaching about adrenalectomy and steroid replacement 2) Pathophysiology exaggerated physiologic action of glucocorticoids Persistent hyperglycemia (or steroid diabetes ) Protein tissue wasting: muscle wasting and weakness Capillary fragility ecchymosis 3) Clinical Manifestations Labs for Cushing s syndrome: hyperglycemia, fluid and electrolyte disturbances, immunosuppressive responses glucose tolerance decreases and glucosuria appears Low ACTH: adrenal tumor as cause of hypercortisolism ACTH levels from petrosal sinuses > ACTH levels from peripheral site (arm): pituitary tumor central ACTH levels (petrosal) = peripheral ACTH levels : ectopic ACTH tumor 6

7 4) Surgical Management Adrenalectomy If no source : bilateral adrenalectomy to interrupt production of cortisol transsphenoidal hypophysectomy: Resection of pituitary tumors large or anatomically complex tumors are excised via a transfrontal approach 85% to 90%: surgical cure rate 5) Nursing Management of the Surgical Client (1) Preoperative Care Risk for Injury: Fractures, Hypertension, or Diabetes Mellitus Prevent Injury: protect from falls and accidents osteoporosis and tend to develop fractures (2) Postoperative Care Assessment Routine postoperative monitoring of shock, addisonian crisis, renal shutdown Risk for Infection Encourage to cough, turn, deep breathe to prevent respiratory tract infection Employ sterile technique with wound care to prevent infection Paralytic ileus is less common 6) Medical Management Medical manage: Inoperable tumors or metastatic tumors radiation therapy, administration of adrenal blocking agents or ACTH-reducing agents (1) Radiation Therapy Internally vs externally (2) Adrenal Blocking Agents interfering ACTH production or adrenal hormone synthesis Mitotane (Lysodren) : cytotoxic antihormonal agent (3) ACTH-Reducing Agents Treatment of hypersecretion by pituitary abnormalities Cyproheptadine (Periactin), bromocriptine, or somatostatin 7) Self-Care Bilateral adrenalectomy : lifelong glucocorticoid replacement Removal of one adrenal gland: daily cortisol replacement until normal function recovery (after 6 to 12 months) 2-2) Hyperaldosteronism most powerful mineralocorticoids conserve sodium, potassium excretion incidence of primary hyperaldosteronism: 1% 7

8 women> men (2 times) frequent in middle-age 1) Etiology and Risk Factors Primary: benigh adrenal lesion Conn s syndrome: hypertension, hypokalemia (in most), hypernatremia, Risk factors for secondary H: chronic heart failure, cirrhosis with ascites, nephrotic syndrome Health promotion: treatment and control of causative disease process 2) Pathophysiology Aldosterone: tubular reabsorption of sodium and water excretion of potassium and hydrogen ions Secondary: high levels of angiotensin II high plasma renin activity Decreased renal perfusion 3) Clinical Manifestations asymptomatic, hypernatremia, hypokalemia complications of chronic hypertension: visual disturbances, heart failure, renal damage, stroke Hypokalemia: muscle weakness, paralysis, cardiac dysrhythmias polyuria polydipsia metabolic alkalosis decrease in ionized calcium tetany and respiratory suppression kidneys escape phenomenon : escape from sodium-retaining and waterretaining action of aldosterone <Diagnosis> Primary: low serum potassium, alkalosis, elevated urinary or plasma aldosterone with low plasma renin 4) Surgical Management treatment of choice for primary hyperaldosteronism Unilateral or bilateral adrenalectomy unilateral: temporary replacement of glucocorticoids bilateral: permanent replacement 5) Nursing Management Administer prescribed medications Closely monitor hypertension or renal damage Preoperative and postoperative management same as hypercortisolism 6) Medical Management receive spironolactone (Aldactone): sodium excretion, treat hypertension and hypokalemia Hypertension: corrected in 4~8 wks 8

9 3) Adrenomedullary Disorders Two tumors in adrenal medulla: pheochromocytoma: causes hyperactivity of the gland 3-1) Pheochromocytoma Catecholamine-secreting tumor of chromaffin cells in adrenalmedulla Rare, 0.1% with diastolic hypertension Equally common in women and men 1) Etiology and Risk Factors Unknown, familial basis 2) Pathophysiology Pheochromocytoma: composed of chromaffin cells cells stain brownish yellow with chromic salts typically benign; fewer than 10% malignant excessive epinephrine and norepinephrine severe manifestations and even death early stage: removed surgically 3) Clinical Manifestations hypertension (elevated BP, headaches) diabetes mellitus (elevated blood glucose and glucosuria) hyperthyroidism (increased metabolic rate, diaphoresis, agitation, PR, emotional outbursts) psychoneurosis (emotional instability) Hypertension: can be persistent, fluctuating, intermittent, or paroxysmal episodes of high BP with pounding headaches <Diagnosis> history and physical examination, chemical tests for catecholamines and metabolites direct assay of catecholamines 4) Surgical Management (1) Adrenalectomy Contraindications before surgery, high BP and vascular complications corrected hypertensive crisis alpha-adrenergic blocking agents: phentolamine(regitine) IV bolus or drip Oral phenoxybenzamine (Dibenzyline) at least 7 days preop to control BP, eliminate paroxy 5) Nursing Management Preop: risk for Injury Promoting rest and relief from stress administering prescribed sedatives 9

10 providing a diet high in vitamins, minerals, and calories Postop: Risk for Injury Monitor and Prevent Shock To prevent posto shock Give IV fluids as prescribed: blood, plasma, dextran, or glucose in water to maintain blood volume Administer IV pressors as prescribed at a rate sufficient to maintain BP within a safe range 10