NCLEX: Endocrine disorders

Endocrine disorders: Hyperparathyroidism

Focus topic: Endocrine disorders

Hyperparathyroidism is characterized by excess activity of one or more of the four parathyroid glands, resulting in excessive secretion of PTH. Such hypersecretion of PTH promotes bone resorption and leads to hypercalcemia and hypophosphatemia. Increased renal and GI absorption of calcium also occurs.

What causes it
Primary hyperparathyroidism may result from a single adenoma, a genetic disorder, or multiple endocrine neoplasias. Secondary hyperparathyroidism may be caused by rickets, vitamin D deficiency, chronic renal failure, or phenytoin (Dilantin) or laxative abuse.

Pathophysiology
Hyperparathyroidism may be primary or secondary. In primary hyperparathyroidism, one or more of the parathyroid glands enlarge, leading to increased PTH secretion and elevated serum calcium levels.

A close second

Focus topic: Endocrine disorders

In secondary hyperparathyroidism, a hypocalcemia-producing abnormality outside the parathyroid gland doesn’t respond to the metabolic action of PTH, leading to excessive compensatory production of PTH.

What to look for
Hyperparathyroidism may produce symptoms. Secondary hyperparathyroidism may produce the same clinical features as primary hyperparathyroidism, with possible skeletal deformities of the long bones (for example, rickets) as well as other symptoms of the underlying disease. Symptoms include:
CNS — psychomotor and personality disturbances, loss of memory for recent events, depression, overt psychosis, stupor and, possibly, coma
GI — anorexia, nausea, vomiting, dyspepsia, and constipation
neuromuscular — fatigue and marked muscle weakness and atrophy, particularly in the legs
renal — signs and symptoms of recurring nephrolithiasis, which may lead to renal insufficiency
skeletal and articular — chronic lower back pain and easy fracturing from bone degeneration, bone tenderness, and joint pain
other — skin pruritus, vision impairment from cataracts, and subcutaneous calcification.

What tests tell you
• Immunoradiometric assay reveals elevated serum PTH levels. This finding, in conjunction with increased serum calcium and decreased phosphorus levels, confirms the diagnosis of hyperparathyroidism.
• X-rays may show diffuse demineralization of bones, bone cysts, outer cortical bone resorption, and subperiosteal erosion of the radial aspect of the middle fingers.
• Laboratory tests reveal elevated urine and serum calcium, chloride, and alkaline phosphatase levels and decreased serum phosphorus levels.
• Secondary hyperparathyroidism is confirmed when serum calcium levels are normal or slightly decreased, with variable serum phosphorus and bicarbonate levels.

How it’s treated
Treatment varies, depending on the cause of the disease. Surgery to remove the adenoma or all but one-half of one gland (the remaining part of the gland is needed to maintain normal PTH levels) is commonly the treatment of choice. Although surgery can relieve bone pain within 3 days, the patient’s renal damage may be irreversible.

Control the calcium

Focus topic: Endocrine disorders

Less invasive treatments are used to decrease calcium levels preoperatively or when surgery isn’t an option. These include:
• forcing fluids
• limiting dietary calcium intake
• promoting sodium and calcium excretion through forced diuresis
• using normal saline solution (up to 6 L in life-threatening situations)

• furosemide (Lasix), or ethacrynic acid (Edecrin)
• administering oral sodium or potassium phosphate, or calcitonin.

Uncover the underlying cause

Focus topic: Endocrine disorders

Treatment for secondary hyperparathyroidism must correct the underlying cause of parathyroid hypertrophy. It includes vitamin D therapy or aluminum hydroxide for hyperphosphatemia in the patient with renal disease. In the patient with chronic secondary hyperparathyroidism, the enlarged glands may not revert to normal size and function even after calcium levels have been controlled; if so, they should be surgically removed.

What to do
• Record intake and output as the patient receives hydration to reduce serum calcium levels.
• Strain urine to check for calculi.
• Monitor sodium, potassium, and magnesium levels frequently.

Listen closely…

Focus topic: Endocrine disorders

• Auscultate for breath sounds often, and be alert for pulmonary edema in the patient receiving large amounts of I.V. saline solution — especially in the presence of pulmonary or cardiac disease.
• Take precautions to avoid falls because the patient is predisposed to pathologic fractures.
• Evaluate the patient. He should understand the need for regular serum calcium level studies, the signs and symptoms of hypercalcemia and hypocalcemia and which ones to report, the reasons for drug therapy and adequate hydration, and possible adverse drug effects.

Endocrine disorders

Endocrine disorders: Hypoparathyroidism

Focus topic: Endocrine disorders

Hypoparathyroidism stems from a deficiency of PTH. Because PTH primarily regulates calcium balance, hypoparathyroidism leads to hypocalcemia and produces neuromuscular signs and symptoms ranging from paresthesia to tetany. The clinical effects are usually correctable with replacement therapy. However, some complications of this disorder, such as cataracts and basal ganglion calcifications, are irreversible.

What causes it
The three major causes of hypoparathyroidism are:
• congenital absence or malfunction of the parathyroid glands
• autoimmune destruction
• removal of or injury to one or more parathyroid glands during neck surgery.

Other causes include:
• ischemic infarction of the parathyroids during surgery or from disease, such as amyloidosis or neoplasms
• suppression of normal gland function caused by hypercalcemia (reversible)
• hypomagnesemia-induced impairment of hormone secretion (reversible)
• massive thyroid radiation therapy (rare).

Pathophysiology
PTH usually maintains serum calcium levels by increasing bone resorption and by stimulating renal conversion of vitamin D to its active form, which enhances GI absorption of calcium and bone resorption. PTH also maintains the inverse relationship between serum calcium and phosphate levels by inhibiting phosphate reabsorption in the renal tubules and enhancing calcium reabsorption. Abnormal PTH production in hypoparathyroidism disrupts this delicate balance.

What to look for
Hypoparathyroidism may not produce symptoms in mild cases. Otherwise, signs and symptoms include:
• neuromuscular irritability
• increased deep tendon reflexes
• positive Chvostek’s and Trousseau’s signs
• dysphagia
• paresthesia
• psychosis.
Other indications include tetany; seizures; arrhythmias; cataracts; abdominal pain; dry, lusterless hair; spontaneous hair loss; brittle fingernails that develop ridges or fall out; possibly dry, scaly skin; and weakened tooth enamel that may cause teeth to stain, crack, and decay easily.

What tests tell you
• Test results that confirm hypoparathyroidism include decreased PTH and serum calcium levels and elevated serum phosphorus levels.
• X-rays reveal increased bone density.
• An ECG shows prolonged QT intervals and QRS-complex and ST-segment changes that are caused by hypocalcemia and may be mistaken for acute MI or conduction abnormalities.

How it’s treated
Therapy includes vitamin D, usually with supplemental calcium. Such therapy is usually lifelong, except for patients with the reversible form of the disease. Types of vitamin D given include dihydrotachysterol if renal function is adequate and calcitriol if renal function is severely compromised.

Call in the calcium cavalry

Focus topic: Endocrine disorders

Acute life-threatening tetany calls for immediate I.V. administration of calcium to raise serum calcium levels. Sedatives and anticonvulsants are given to control spasms until calcium levels rise. Chronic tetany calls for vitamin D and possibly oral calcium supplements to maintain normal serum calcium levels.

What to do
• While awaiting diagnosis of hypoparathyroidism in a patient with a history of tetany, maintain a patent I.V. line and keep 10% calcium gluconate solution available.
• Institute seizure precautions because the patient is at risk for seizures.
• Keep a tracheostomy tray and an endotracheal tube at the bedside because laryngospasm may result from hypocalcemia.
• Monitor for Chvostek’s and Trousseau’s signs.
• For the patient with tetany, prepare to administer 10% calcium gluconate by slow I.V. infusion and maintain a patent airway. Prepare the patient for transport to the ICU according to facility policy because the patient may also require intubation and sedation with I.V. diaze pam (Valium). Monitor vital signs often, especially if the patient received I.V. diazepam, to make sure his blood pressure and heart rate return to normal.
• When caring for the patient with hypoparathyroidism, stay alert for minor muscle twitching (especially in the hands) and for signs of laryngospasm (respiratory stridor or dysphagia). These effects may signal the onset of tetany.

Toxic trouble

Focus topic: Endocrine disorders

• Because the patient with chronic disease has prolonged QT intervals on an ECG, watch for ventricular arrhythmias, heart block, and signs of decreased cardiac output. Closely monitor the patient who receives digoxin (Lanoxin) and calcium because calcium potentiates the effect of digoxin. Watch for signs and symptoms of digoxin toxicity (arrhythmias, nausea, fatigue, changes in vision).
• Evaluate the patient. He shouldn’t develop tetany, and his serum calcium levels should be normal. The patient should understand the signs and symptoms of hypocalcemia and hypercalcemia and state which ones to report; identify high-calcium, low-phosphorus foods; and understand the importance of good nail grooming and the need for emollient creams to soften the skin.

Endocrine disorders

Endocrine disorders: Hyperthyroidism

Focus topic: Endocrine disorders

Hyperthyroidism is a metabolic imbalance that results from excessive thyroid hormone. The most common form of hyperthyroidism is Graves’ disease (thyrotoxicosis), which increases T4 production, enlarges the thyroid gland (goiter), and causes multisystem changes. With treatment, most patients can lead normal lives. However, thyroid storm — an acute exacerbation of hyperthyroidism — is a medical emergency that may lead to heart failure.

What causes it
Graves’ disease is an autoimmune disease and is usually familial. Thyroid receptor antibodies occur in most patients with this disorder.

Pathophysiology
In Graves’ disease, thyroid-stimulating antibodies bind to and stimulate the TSH receptors of the thyroid gland. The trigger for this autoimmune response is unclear. Graves’ disease is also associated with the production of several autoantibodies formed because of a defect in suppressor T-lymphocyte function.

What to look for
Classic signs and symptoms of Graves’ disease include:
• diffusely enlarged thyroid
• nervousness
• heat intolerance
• weight loss despite increased appetite
• sweating
• diarrhea
• tremor
• palpitations
• possibly exophthalmos.

Endocrine disorders

 

In thyroid storm, these signs and symptoms can be accompanied by extreme irritability, hypertension, tachycardia, vomiting, temperature up to 106º F (41.1º C), delirium, and coma. Other signs and symptoms include:
cardiovascular system — tachycardia; full, bounding pulse; wide pulse pressure; cardiomegaly; increased cardiac output and blood volume; a visible point of maximal impulse; paroxysmal supraventricular tachycardia and atrial fibrillation (found especially in elderly patients); occasionally, a systolic murmur at the left sternal border
CNS — difficulty concentrating, excitability or nervousness, fine tremor, shaky handwriting, clumsiness, and mood swings ranging from occasional outbursts to overt psychosis
eyes — exophthalmos; occasional inflammation of conjunctivae, corneas, or eye muscles; diplopia; increased tearing; lid lag; lid retraction
GI — increased appetite but occasional anorexia, especially in elderly patients; increased defecation; soft stools or, with severe disease, diarrhea; liver enlargement
musculoskeletal system — weakness, fatigue, and proximal muscle atrophy; periodic paralysis, especially in Asian and Latino males; occasional acropachy (soft-tissue swelling), accompanied by underlying bone changes where new bone formation occurs

reproductive system — in females, oligomenorrhea or amenorrhea, decreased fertility, higher incidence of spontaneous abortions; in males, gynecomastia
respiratory system — dyspnea on exertion and, possibly, at rest
skin, hair, and nails — smooth, warm, flushed paper-thin skin; pretibial myxedema (dermopathy), producing thickened skin, accentuated hair follicles, and raised red patches of skin that are itchy and sometimes painful, with occasional nodule formation; fine, soft hair; premature graying and increased hair loss in both sexes; friable nails and Plummer’s nails (distal nail separated from the bed).

What tests tell you
• Radioimmunoassay test shows elevated T4 levels.
• Thyroid scan reveals increased 131I uptake.
• Immunometric a ssay shows suppressed sensitive TSH levels.
• Orbital sonography and CT scan show subclinical ophthalmopathy.

How it’s treated
The primary forms of treatment for hyperthyroidism are antithyroid drugs, 131I, beta-adrenergic blockers, sedation, and surgery. Appropriate treatment depends on the size of the goiter, the causes, the patient’s age and parity, and how long surgery (if planned) will be delayed. Treatment includes:
• Antithyroid drug therapy with propylthiouracil (PTU) and methimazole blocks thyroid hormone synthesis. It’s used for pregnant women and patients who refuse surgery or 131I treatment.
• Another major form of therapy for hyperthyroidism is a single oral dose of 131I. After ablative treatment with 131I or surgery, patients require regular, frequent medical supervision for the rest of their lives. They usually develop hypothyroidism, sometimes several years after treatment.

Rein in those hormones

Focus topic: Endocrine disorders

• Partial thyroidectomy is indicated for the patient with a very large goiter, whose hyperthyroidism has repeatedly relapsed after drug therapy. Subtotal thyroidectomy removes part of the thyroid gland, decreasing its size and capacity for hormone production and storage.
• Before surgery, the patient may receive iodides (Lugol’s solution or saturated solution of potassium iodide), antithyroid drugs, or high doses of propranolol, a beta-adrenergic blocker, to help prevent thyroid storm. If euthyroidism isn’t achieved, surgery is delayed and the patient receives propranolol to decrease systemic effects (such as cardiac arrhythmias) caused by hyperthyroidism.
• During pregnancy, PTU is the preferred therapy. In pregnant patients, anti thyroid medication should be limited to the minimum dosage required to keep maternal thyroid function testing at highnormal or slightly elevated levels. About 1% of infants born to mothers receiving antithyroid medication have hypothyroidism.

Steroid injections

Focus topic: Endocrine disorders

• Therapy for hyperthyroid ophthalmopathy includes local applications of topical medications but may also require high doses of corticosteroids given systemically or, in severe cases, injected into the retrobulbar area.
• A patient with severe exophthalmos that causes pressure on the optic nerve may require surgical decompression to lessen pressure on the orbital contents.
• Treatment for thyroid storm includes an antithyroid drug such as PTU, I.V. propranolol to block sympathetic effects, a corticosteroid to replace depleted cortisol levels, and an iodide to block release of thyroid hormone. Supportive measures include nutrients, vitamins, fluid administration, and sedation, as necessary.

What to do
• Provide vigilant care to prevent acute exacerbations and complications:
– Record vital signs and weight.
– Monitor serum electrolyte levels and check periodically for hyperglycemia and glycosuria.
– Carefully monitor cardiac function.
– Check LOC and urine output.
• If the patient is in her first trimester of pregnancy, report signs and symptoms of spontaneous abortion (spotting and occasional mild cramps) to the doctor immediately.
• Remember, extreme nervousness may produce bizarre behavior. Reassure the patient and his family that such behavior subsides with treatment. Provide sedatives as necessary.
• To promote weight gain, provide a high-protein, high-calorie diet, with six meals per day and vitamin supplements. Suggest a low-sodium diet for the patient with edema.

Storm watch

Focus topic: Endocrine disorders

• Watch for signs of thyroid storm. Check intake and output carefully to ensure adequate hydration and fluid balance. Closely monitor blood pressure, cardiac rate and rhythm, and body temperature. If the patient has a high fever, reduce it with appropriate hypothermic measures (sponging, hypothermia blankets, and ac eta- minophen); avoid aspirin because it raises T4 levels. Maintain an I.V. line and give drugs, as ordered.

• If iodine is part of the treatment, mix it with water or juice to prevent GI distress, and administer it through a straw to prevent tooth discoloration.
• If the patient underwent thyroidectomy, provide meticulous postoperative care to prevent complications.
• Evaluate the patient. He should maintain adequate fluid volume and electrolyte balance, normal cardiac function, normal body temperature, and adequate weight (preferably, he’ll gain weight); his eyes should be as comfortable as possible and free from corneal damage; thyroid storm should be prevented. He will understand the need for regular medical follow-up and will schedule return appointments. If he takes an antithyroid drug or is on 131I therapy, he’ll know which signs and symptoms to report to his practitioner and will have a sheet that lists them.

Endocrine disorders

Endocrine disorders: Hypothyroidism

Focus topic: Endocrine disorders

A state of low serum thyroid hormone levels or cellular resistance to thyroid hormone, hypothyroidism results from hypothalamic, pituitary, or thyroid insufficiency. Hypothyroidism is most prevalent in women and can progress to life-threatening myxedema coma — usually precipitated by infection, exposure to cold, or sedatives.

What causes it
Hypothyroidism may result from:
• thyroidectomy
• radiation therapy
• chronic autoimmune thyroiditis (Hashimoto’s disease)
• inflammatory conditions, such as amyloidosis and sarcoidosis
• pituitary failure to produce TSH
• hypothalamic failure to produce thyrotropin-r eleasing hormone (TRH)
• inborn errors of thyroid hormone synthesis
• inability to synthesize thyroid hormone because of iodine deficiency (usually dietary)
• use of antithyroid medications such as PTU.

Pathophysiology
In primary hypothyroidism, a decrease in thyroid hormone production is a result of the loss of thyroid tissue. This results in an increased secretion of TSH that leads to a goiter. In secondary hypothyroidism, typically the pituitary fails to synthesize or secrete adequate amounts of TSH, or target tissues fail to respond to normal blood levels of thyroid hormone. Either type may progress to myxedema, which is clinically more severe and considered a medical emergency.

Endocrine disorders

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What to look for
Signs and symptoms of hypothyroidism include:
• weakness, fatigue
• forgetfulness
• cold intolerance
• unexplained weight gain
• constipation
• goiter
• slow speech
• decreasing mental stability
• cool, dry, coarse, flaky, inelastic skin

• puffy face, hands, and feet; periorbital edema
• dry, sparse hair
• thick, brittle nails.
Other indications include a slow pulse rate, anorexia, abdominal distention, menorrhagia, decreased libido, infertility, ataxia, intention tremor, nystagmus, and delayed reflex relaxation time (especially in the Achilles tendon).
Clinical effects of myxedema coma include progressive stupor, hypoventilation, hypoglycemia, hyponatremia, hypotension, and hypothermia.

What tests tell you
• Radioimmunoassay tests showing low T3 and T4 levels indicate hypothyroidism.
• The TSH level increases with primary hypothyroidism and decreases in secondary hypothyroidism. The TRH level is decreased in hypothalamic insufficiency.
• Serum cholesterol, carotene, alkaline phosphatase, and triglyceride levels are increased.
• In myxedema coma, laboratory tests may also show low serum sodium levels and decreased pH and increased partial pressure of carbon dioxide in arterial blood, indicating respiratory acidosis.

How it’s treated
Therapy for hypothyroidism consists of gradual thyroid replacement with levothyroxine (Synthroid). Effective treatment of myxedema coma supports vital functions while restoring euthyroidism. To support blood pressure and pulse rate, the patient receives I.V. levothyroxine, plus hydrocortisone in cases of pituitary or adrenal insufficiency. Hypoventilation requires oxygenation and vigorous respiratory support. Other supportive measures include careful fluid replacement and antimicrobial medications for infection.

What to do
• Provide a high-bulk, low-calorie diet and encourage activity.
• Administer cathartics and stool softeners as needed.
• After thyroid replacement therapy begins, watch for signs of hyperthyroidism, such as restlessness, sweating, and excessive weight loss.
• Advise the patient how to obtain medical identification jewelry.
• Evaluate the patient. She should have a normal bowel elimination pattern and adequate cardiac function, know which cardiac symptoms to report, and understand the need for lifelong thyroid replacement and regular medical care to monitor replacement therapy. She should have medical identification jewelry and a wallet identification card. She should show signs of adequate cardiac output and function, including normal blood pressure and pulse rate, adequate urine output, intact skin, adequate fluid volume and electrolyte balance, and adequate gas exchange.

Endocrine disorders

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