Republic of the Philippines

ISABELA STATE UNIVERSITY

City of Ilagan Campus

COLLEGE OF NURSING

NUR 322 (Care of the Clients with Endocrine Disorders)

Subject Professor: CHARLES Z. ARIOLA JR., LPT, RN, CRN, MSN, MAN.

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

- 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:
1. numbness,
2. tingling, and cramps in the extremities,
3. 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.