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The Parathyroid Glands

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Republic of the Philippines

ISABELA STATE UNIVERSITY


City of Ilagan Campus

COLLEGE OF NURSING
NUR 322 (Care of the Clients with Endocrine Disorders)

THE PARATHYROID GLANDS


Anatomic and Physiologic Overview

- The parathyroid glands (normally four) are situated in the neck and embedded in the posterior aspect of the
thyroid gland.
- Parathormone (parathyroid hormone), the protein hormone produced by the parathyroid glands, regulates
calcium and phosphorus metabolism.
- Increased secretion of parathormone results in increased calcium absorption from the kidney, intestine, and
bones, which raises the blood calcium level.
- Some actions of this hormone are increased by the presence of vitamin D.
- Parathormone also tends to lower the blood phosphorus level.
- The serum level of ionized calcium regulates the output of parathormone. Increased serum calcium results in
decreased parathormone secretion, creating a negative feedback system

DISORDERS OF THE PARATHYROID GLANDS

HYPERPARATHYROIDISM
- Hyperparathyroidism, which is caused by overproduction of parathormone by the parathyroid glands
- Characterized by bone decalcification and the development of renal calculi (kidney stones) containing calcium.
- Primary hyperparathyroidism
-
- occurs two to four times more often in women than in men and is most common in people between 60 and 70
years of age.
- Its incidence is approximately 25 cases per 100,000.
- The disorder is rare in children younger than 15 years of age, but its incidence increases 10-fold between the ages
of 15 and 65 years. Half of the people diagnosed with hyperparathyroidism do not have symptoms.
Secondary Hyperparathyroidism

- Secondary hyperparathyroidism, with manifestations similar to those of primary hyperparathyroidism, occurs in


patients who have chronic renal failure and so-called renal rickets as a result of phosphorus retention, increased
stimulation of the parathyroid glands, and increased parathormone secretion
CLINICAL MANIFESTATIONS

- The patient may have no symptoms or may experience signs and symptoms resulting from involvement of several
body systems which include:
1. Apathy
2. Fatigue
3. Muscle Weakness
4. Nausea
5. Vomiting
6. Constipation
7. Hypertension
8. Cardiac Dysrhythmias
- All these signs and symptoms are attributable to the increased concentration of calcium in the blood.
- Psychological effects may vary from irritability and neurosis to psychoses caused by the direct action of calcium
on the brain and nervous system.
- An increase in calcium produces a decrease in the excitation potential of nerve and muscle tissue.
- The formation of stones in one or both kidneys, related to the increased urinary excretion of calcium and
phosphorus, is one of the important complications of hyperparathyroidism and occurs in 55% of patients with
primary hyperparathyroidism.
- Renal damage results from the precipitation of calcium phosphate in the renal pelvis and parenchyma, which
causes renal calculi (kidney stones), obstruction, pyelonephritis, and renal failure.
- Musculoskeletal symptoms accompanying hyperparathyroidism may be caused by demineralization of the bones
or by bone tumors composed of benign giant cells resulting from overgrowth of osteoclasts.
- The patient may develop skeletal pain and tenderness, especially of the back and joints; pain on weight bearing;
pathologic fractures; deformities; and shortening of body stature.
- Bone loss attributable to hyperparathyroidism increases the risk of fracture. The incidence of peptic ulcer and
pancreatitis is increased with hyperparathyroidism and may be responsible for many of the GI symptoms that
occur.
ASSESSMENT AND DIAGNOSTIC FINDINGS

- Primary hyperparathyroidism is diagnosed by persistent elevation of serum calcium levels and an elevated
concentration of parathormone.
- Radioimmunoassays for parathormone are sensitive and differentiate primary hyperparathyroidism from other
causes of hypercalcemia in more than 90% of patients with elevated serum calcium levels.
- An elevated serum calcium level alone is a nonspecific finding, because serum levels may be altered by diet,
medications, and renal and bone changes.
- Bone changes may be detected on x-ray or bone scans in advanced disease.
- The double-antibody parathyroid hormone test is used to distinguish between primary hyperparathyroidism and
malignancy as a cause of hypercalcemia.
- Ultrasound, MRI, thallium scan, and fine-needle biopsy have been used to evaluate the function of the
parathyroids and to localize parathyroid cysts, adenomas, or hyperplasia.
MEDICAL MANAGEMENT
A. Surgical Management
- The recommended treatment for primary hyperparathyroidism is the surgical removal of abnormal parathyroid
tissue (parathyroidectomy) (Rodgers, Lew & Solorzano, 2008; Suliburk & Perrier, 2007).
- In the past, the standard parathyroidectomy involved a bilateral neck exploration under general anesthesia.
- Today, minimally invasive parathyroidectomy techniques allow for unilateral neck exploration using local
anesthesia; these are performed on an outpatient basis.
- In some cases only the removal of a single diseased gland is necessary, reducing morbidity rates associated with
surgery.
- For asymptomatic patients who have only mildly elevated serum calcium concentrations and normal renal
function, surgery may be delayed and the patient monitored closely for worsening of hypercalcemia, bone
deterioration, renal impairment, or the development of kidney stones.
- Surgery is recommended for asymptomatic patients who meet the following criteria:
(1) younger than 50 years of age,
(2) unable or unlikely to participate in follow-up care,
(3) serum calcium level more than 1.0 mg/dL (0.25 mmol/L) above normal reference range,
(4) urinary calcium level greater than 400 mg/day (10 mmol/day),
(5) a 30% or greater decrease in renal function,
(6) with complaints of primary hyperparathyroidism, including nephrocalcinosis, osteoporosis, or a severe
psychoneurologic disorder.
- However, according to several authors, these criteria are too conservative; there is little evidence to support
longterm medical management of asymptomatic patients who do not meet these criteria (Rodgers, et al., 2008;
Suliburk & Perrier, 2007).

B. Hydration Therapy
- Because kidney involvement is possible, patients with hyperparathyroidism are at risk for renal calculi. Therefore,
a daily fluid intake of 2000 mL or more is encouraged to help prevent calculus formation.
- Cranberry juice is suggested, because it may lower the urinary pH. It can be added to other juices or to ginger ale
for variety. Cranberry extract tablets are an alternative to reduce urinary pH. The patient is instructed to report
other manifestations of renal calculi, such as abdominal pain and hematuria.
- Thiazide diuretics are avoided, because they decrease the renal excretion of calcium and further elevate serum
calcium levels.
- Because of the risk of hypercalcemic crisis, the patient is instructed to avoid dehydration and to seek immediate
health care if conditions that commonly produce dehydration (eg, vomiting, diarrhea) occur.

C. MOBILITY
 Mobility of the patient, with walking or use of a rocking chair for those with limited mobility, is encouraged as much
as possible, because bones that are subjected to normal stress give up less calcium.
 Bed rest increases calcium excretion and the risk for renal calculi.
 Oral phosphates lower the serum calcium level in some patients; long-term use is not recommended because of the
risk of ectopic calcium phosphate deposition in soft tissues

D. DIET AND MEDICATIONS


 Nutritional needs are met, but the patient is advised to avoid a diet with restricted or excess calcium.
 If the patient has a coexisting peptic ulcer, prescribed antacids and protein feedings are necessary.
 Because anorexia is common, efforts are made to improve the appetite.
 Prune juice, stool softeners, and physical activity, along with increased fluid intake, help offset constipation, which is
common postoperatively.

NURSING MANAGEMENT
 The insidious onset and chronic nature of hyperparathyroidism and its diverse and commonly vague symptoms may
result in depression and frustration.
 The family may have considered the patient’s illness to be psychosomatic.
 An awareness of the course of the disorder and an understanding approach by the nurse may help the patient and
family deal with their reactions and feelings
 The nursing management of the patient undergoing parathyroidectomy is essentially the same as that of a patient
undergoing thyroidectomy. However, the previously described precautions about airway patency, dehydration,
immobility, and diet are particularly important in the patient who is awaiting or recovering from parathyroidectomy.
 Although not all parathyroid tissue is removed during surgery in an effort to control the calcium–phosphorus balance,
the nurse closely monitors the patient to detect symptoms of tetany (which may be an early postoperative
complication).
 Most patients quickly regain function of the remaining parathyroid tissue and experience only mild, transient
postoperative hypocalcemia.
 In patients with significant bone disease or bone changes, a more prolonged period of hypocalcemia should be
anticipated.
 The nurse reminds the patient and family about the importance of follow-up to ensure return of serum calcium levels
to normal.
COMPLICATIONS
 Acute hypercalcemic crisis can occur with extreme elevation of serum calcium levels.
 Serum calcium levels greater than 15 mg/dL (3.7 mmol/L) result in neurologic, cardiovascular, and renal symptoms
that can be life-threatening.
 Treatment includes rehydration with large volumes of IV fluids, diuretic agents to promote renal excretion of excess
calcium, and phosphate therapy to correct hypophosphatemia and decrease serum calcium levels by promoting
calcium deposition in bone and reducing the gastrointestinal absorption of calcium.
 Cytotoxic agents (eg, mithramycin), calcitonin, and dialysis may be used in emergency situations to decrease serum
calcium levels quickly
 A combination of calcitonin and corticosteroids has been administered in emergencies to reduce the serum calcium
level by increasing calcium deposition in bone.
 Other agents that may be administered to decrease serum calcium levels include bisphosphonates (eg, etidronate
[Didronel], pamidronate [Aredia]).
 Expert assessment and care are required to minimize complications and reverse the life-threatening hypercalcemia.
Medications are administered with care, and attention is given to fluid balance to promote return of normal fluid and
electrolyte balance. Supportive measures are necessary for the patient and family.
NURSING ALERT
 The patient in acute hypercalcemic crisis requires close monitoring for life-threatening complications and prompt
treatment to reduce serum calcium levels.

HYPOPARATHYROIDISM
 The most common cause of hypoparathyroidism is inadequate secretion of parathormone after interruption of the
blood supply or surgical removal of parathyroid gland tissue during thyroidectomy, parathyroidectomy, or radical
neck dissection.
 These small glands are easily overlooked and can be removed inadvertently during thyroid surgery.
 Atrophy of the parathyroid glands of unknown cause is a less common cause of hypoparathyroidism.
 Deficiency of parathormone results in increased blood phosphate (hyperphosphatemia) and decreased blood calcium
(hypocalcemia) levels.
 In the absence of parathormone, there is decreased intestinal absorption of dietary calcium and decreased resorption
of calcium from bone and through the renal tubules.
 Decreased renal excretion of phosphate causes hypophosphaturia, and low serum calcium levels result in
hypocalciuria

Clinical Manifestations
 Hypocalcemia causes irritability of the neuromuscular system and contributes to the chief symptom of
hypoparathyroidism—tetany.
 Tetany is a general muscle hypertonia, with tremor and spasmodic or uncoordinated contractions occurring with or
without efforts to make voluntary movements.
 Symptoms of latent tetany are:
numbness,
1. tingling, and cramps in the extremities,
2. stiffness in the hands and feet.
- In overt tetany, the signs include:
1. bronchospasm,
2. laryngeal spasm,
3. carpopedal spasm (flexion of the elbows and wrists and extension of the carpophalangeal joints and
dorsiflexion of the feet),
4. dysphagia,
5. photophobia,
6. cardiac dysrhythmias,
7. seizures.
- Other symptoms include:
1. anxiety,
2. irritability,
3. depression
4. delirium.
5. ECG changes and hypotension also may occur
Assessment and Diagnostic Findings
 A positive Trousseau’s sign or a positive Chvostek’s sign suggests latent tetany.
 Trousseau’s sign is positive when carpopedal spasm is induced by occluding the blood flow to the arm for 3 minutes
with a blood pressure cuff.
 Chvostek’s sign is positive when a sharp tapping over the facial nerve just in front of the parotid gland and anterior to
the ear causes spasm or twitching of the mouth, nose, and eye. The diagnosis of hypoparathyroidism often is difficult
because of the vague symptoms, such as aches and pains.
 Therefore, laboratory studies are especially helpful.
 Tetany develops at serum calcium levels of 5 to 6 mg/dL (1.2 to 1.5 mmol/L) or lower.
 Serum phosphate levels are increased, and x-rays of bone show increased density.
 Calcification is detected on x-rays of the subcutaneous or paraspinal basal ganglia of the brain.

Medical Management
 The goal of therapy is to increase the serum calcium level to 9 to 10 mg/dL (2.2 to 2.5 mmol/L) and to eliminate the
symptoms of hypoparathyroidism and hypocalcemia.
 When hypocalcemia and tetany occur after a thyroidectomy, the immediate treatment is administration of IV calcium
gluconate. If this does not decrease neuromuscular irritability and seizure activity immediately, sedative agents such
as pentobarbital may be administered.
 Parenteral parathormone can be administered to treat acute hypoparathyroidism with tetany. However, the high
incidence of allergic reactions to injections of parathormone limits its use to acute episodes of hypocalcemia.
 The patient receiving parathormone is monitored closely for allergic reactions and changes in serum calcium levels.
 Because of neuromuscular irritability, the patient with hypocalcemia and tetany requires an environment that is free
of noise, drafts, bright lights, or sudden movement.
 Tracheostomy or mechanical ventilation may become necessary, along with bronchodilating medications, if the
patient develops respiratory distress.
 Therapy for chronic hypoparathyroidism is determined after serum calcium levels are obtained.
 A diet high in calcium and low in phosphorus is prescribed. Although milk, milk products, and egg yolk are high in
calcium, they are restricted because they also contain high levels of phosphorus.
 Spinach also is avoided because it contains oxalate, which would form insoluble calcium substances.
 Oral tablets of calcium salts, such as calcium gluconate, may be used to supplement the diet.
 Aluminum hydroxide gel or aluminum carbonate (Gelusil, Amphojel) also is administered after meals to bind
phosphate and promote its excretion through the GI tract.
 Variable dosages of a vitamin D preparation—dihydrotachysterol (AT 10 or Hytakerol), ergocalciferol (vitamin D),
or cholecalciferol (vitamin D)—are usually required and enhance calcium absorption from the GI tract.

Nursing Management
 Nursing management of the patient with possible acute hypoparathyroidism includes the following:
• Care of postoperative patients who have undergone thyroidectomy, parathyroidectomy, or radical neck
dissection is directed toward detecting early signs of hypocalcemia and anticipating signs of tetany, seizures, and
respiratory difficulties.
• Calcium gluconate is kept at the bedside with equipment necessary for emergency IV administration. If the
patient requiring administration of calcium gluconate has a cardiac disorder, is subject to dysrhythmias, or is
receiving digitalis, the calcium gluconate is administered slowly and cautiously.
• Calcium and digitalis increase systolic contraction and also potentiate each other; this can produce potentially
fatal dysrhythmias. Consequently, the cardiac patient requires continuous cardiac monitoring and careful
assessment.

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