MEDICAL-SURGICAL NURSING┃MIDTERMS┃TRANS 2
MANAGEMENT OF CLIENTS WITH THYROID AND
PARATHYROID DISORDERS
MRS. TINA JOY G. MANTE, RN, MAN┃FEB 21, 2022
TRANSCRIBED BY TOM CUENCA
THYROID GLAND
• The thyroid gland—the largest endocrine gland—is a butterfly-
shaped organ located in the lower neck, anterior to the trachea (Fig.
52-3).
• It consists of two lateral lobes connected by an isthmus.
• The gland is about 5 cm long and 3 cm wide and weighs about 30
g.
• The blood flow to the thyroid is very high (about 5 mL/min per gram
of thyroid tissue), approximately five times the blood flow to the
liver.
• Blood and nerve supply and lymphatic drainage is composed
of the following:
Arterial supply: superior thyroid artery and inferior thyroid artery
Venous supply: superior thyroid vein and inferior vein
Nerve supply: superior laryngeal nerve and recurrent laryngeal
nerve
Lymphatic drainage: lateral deep cervical lymph node and pre-
tracheal or paratracheal lymph nodes
• The thyroid gland produces three hormones: thyroxine (T4),
triiodothyronine (T3), and calcitonin.
ANATOMIC AND PHYSIOLOGIC REVIEW OF THE THYROID
GLAND
• Various hormones and chemicals are responsible for normal thyroid
function. Key among them are thyroid hormone, calcitonin, and
iodine.
THYROID HORMONE
• Thyroid hormone is comprised of T4 and T3, two separate
hormones produced by the thyroid gland. Both are amino acids that
contain iodine molecules bound to the amino acid structure; T4
contains four iodine atoms in each molecule, and T3 contains three.
• These hormones are synthesized and stored bound to proteins in
the cells of the thyroid gland until needed for release into the
bloodstream.
• Three thyroid binding hormones—thyroxine-binding globulin
(TBG), transthyretin (formerly known as thyroid-binding
prealbumin), and albumin—bind and transport T3 and T4 (Porth
2015).
SYNTHESIS OF THYROID HORMONE
• Iodine is essential to the thyroid gland for synthesis of its hormones.
The major use of iodine in the body is by the thyroid, and the major
derangement in iodine deficiency is alteration of thyroid function.
• Iodide is ingested in the diet and absorbed into the blood in the GI
tract.
• The thyroid gland is extremely efficient at taking up iodide from the
blood and concentrating it within the cells, where iodide ions are
converted to iodine molecules, which react with tyrosine (an amino
acid) to form the thyroid hormones (Salvatore, Davies, Sclumberger,
et al., 2016).
REGULATION OF THYROID HORMONE
• The secretion of T3 and T4 by the thyroid gland is controlled by TSH
(also called thyrotropin) from the anterior pituitary gland.
• TSH controls the rate of thyroid hormone release through a
negative feedback mechanism. In turn, the level of thyroid
hormone in the blood determines the release of TSH. If the thyroid
hormone concentration in the blood decreases, the release of TSH
increases, which causes increased output of T3 and T4.
• The term euthyroid refers to thyroid hormone production that is
normal.
• TRH, secreted by the hypothalamus, exerts a modulating influence
on the release of TSH from the pituitary. Environmental factors,
such as a decrease in temperature, may lead to increased secretion
of TRH, resulting in elevated secretion of thyroid hormones.
• The figure below shows the hypothalamic–pituitary–thyroid axis,
which regulates thyroid hormone production.
• Thyroid-releasing hormone (TRH) from the hypothalamus
stimulates the pituitary gland to secrete thyroid-stimulating
hormone (TSH). TSH stimulates the thyroid to produce thyroid
hormone (triiodothyronine [T3] and thyroxine [T4]). High
circulating levels of T3 and T4 inhibit further TSH secretion and
thyroid hormone production through a negative feedback
mechanism (dashed lines).
FUNCTION OF THYROID HORMONE
• The main function of thyroid hormone is to control cellular metabolic
activity.
• T4, a relatively weak hormone, maintains body metabolism in a
steady state.
• T3 is about five times as potent as T4 and has a more rapid
metabolic action.
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• These hormones accelerate metabolic processes by increasing the
level of specific enzymes that contribute to oxygen consumption and
altering the responsiveness of tissues to other hormones.
• The thyroid hormones influence cell replication and are important in
brain development. Thyroid hormone is also necessary for normal
growth.
• Thyroid hormones affect virtually every major organ system and
tissue function, including the basal metabolic rate, tissue
thermogenesis, serum cholesterol levels, and vascular resistance
(Porth, 2015).
CALCITONIN
• Calcitonin, or thyrocalcitonin, is another important hormone
secreted by the thyroid gland.
• It is secreted in response to high plasma levels of calcium, and it
reduces the plasma level of calcium by increasing its deposition in
bone.
PATHOPHYSIOLOGY
• Inadequate secretion of thyroid hormone during fetal and neonatal
development results in intellectual disability and stunted
physical growth (congenital hypothyroidism) because of
general depression of metabolic activity (LaFranchi, 2016).
• In adults, hypothyroidism manifests as lethargy, slow mentation,
weight gain, constipation, cold intolerance, and generalized
slowing of body functions (Surks, 2016a).
• Oversecretion of thyroid hormones (hyperthyroidism) is manifested
by a greatly increased metabolic rate. Many of the other
characteristics of hyperthyroidism result from the increased
response to circulating catecholamines (epinephrine and
norepinephrine).
• Oversecretion of thyroid hormones is usually associated with an
enlarged thyroid gland known as a goiter.
• Goiter also commonly occurs with iodine deficiency. In this latter
condition, lack of iodine results in low levels of circulating thyroid
hormones, which causes increased release of TSH; the elevated
TSH causes overproduction of thyroglobulin (a precursor of T3 and
T4) and hypertrophy of the thyroid gland.
THYROID DISORDERS
HYPERTHYROIDISM GRAVE’S DISEASE
THYROID STORM (THYROTOXIC
CRISIS)
TOXIC THYROID NODULE
HYPOTHYROIDISM HASHIMOTO’S THYROIDITIS
CRETINISM
MYXOEDEMA
POSTPARTUM THYROIDITIS
SUBACUTE THYROIDITIS
SICK EUTHYROIDISM
HYPERTHYROIDISM
• Hyperthyroidism is excessive thyroid hormone secretion from the
thyroid gland.
• The manifestations of hyperthyroidism are called thyrotoxicosis,
regardless of the origin of the thyroid hormones. This term is correct
even when a person takes a large amount of synthetic thyroid
hormones that manifests as thyrotoxicosis although he or she does
not have hyperthyroidism.
• Thyroid hormones increase metabolism in all body organs,
producing many different manifestations.
• Hyperthyroidism can be temporary or permanent, depending on
the cause.
• The excessive thyroid hormones stimulate most body systems,
causing hypermetabolism and increased sympathetic nervous
system activity.
THYROTOXICOSIS
• Hyperthyroidism, a common endocrine disorder, is a form of
thyrotoxicosis resulting from an excessive synthesis and secretion
of endogenous or exogenous thyroid hormones by the thyroid
(Bahn, Burch, Cooper, et al., 2011)
• Hypermetabolic clinical syndrome resulting from serum elevation
of thyroid hormone levels (T3 and T4).
• Causes are Graves’ disease, multinodular goiter and toxic
adenoma. Other causes include thyroiditis (inflammation of the
thyroid gland) and excessive ingestion of thyroid hormone.
• Graves’ disease is the most common form.
GRAVE’S DISEASE
• Graves’ disease, the most common cause of hyperthyroidism, is
an autoimmune disorder that results from an excessive output of
thyroid hormones caused by abnormal stimulation of the thyroid
gland by circulating immunoglobulins (Bahn et al., 2011; Muldoon,
Mai, & Burch, 2014).
• This disease affects women eight times more frequently than men,
with onset usually between the second and fourth decades.
• The disorder may appear after an emotional shock, stress, or an
infection, but the exact significance of these relationships is not
understood.
• Hyperthyroidism has many causes. The most common form of the
disease is Graves' disease, also called toxic diffuse goiter.
• Graves' disease is an autoimmune disorder resulting from
Hashimoto's thyroiditis (HT) (Mandel et al., 2011). HT results in
the production of autoantibodies to different substances and
structures within the thyroid gland.
• In Graves' disease, these antibodies (thyroid-stimulating
immunoglobulins [TSIs]) attach to the thyroid-stimulating
hormone (TSH) receptors on the thyroid tissue. The thyroid gland
responds by increasing the glandular cells, which enlarges the
gland, forming a goiter, and overproduces thyroid hormones
(thyrotoxicosis).
• When HT causes production of antibodies to other structures within
the thyroid gland, hypothyroidism results.
• In Graves' disease, all the general manifestations of
hyperthyroidism are present. In addition, other manifestations
specific to Graves' disease may occur, including exophthalmos
(abnormal protrusion of the eyes) and pretibial myxedema (dry,
waxy swelling of the front surfaces of the lower legs that resembles
benign tumors or keloids). Not all patients with a goiter have
hyperthyroidism.
SIGNS AND SYMPTOMS
1. Exophthalmus
2. Photophobia, eyelid retraction (eyelid lag) and globe (eyeball) lag
3. Skin is warm and moist, palms are warm, moist and hyperemic and
Plummer’s nails are seen
4. Pretibial myxedema
5. Alopecia and vitiligo
6. Severe cases proptosis may be seen
7. Excessive sweating and heat intolerance
8. CVS symptoms include: palpitations, CCF (congestive cardiac
failure), and isolated systolic hypertension
9. Metabolic symptoms include: weight loss despite of increased in
appetite
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10. GIT symptoms include: hyper-defecation • Excess production of thyroid hormones from functionally
11. Exacerbate bronchial asthma autonomous thyroid nodules which do not require the stimulation
12. CNS symptoms: nervousness, irritability, tremor, insomnia, and from TSH.
proximal muscle weakness • It is the second common cause of hyperthyroidism.
13. In females: amenorrhea or oligomenorrhea • Occurs in individuals over 60 years of age and females are mostly
14. In males: impotence and loss of libido affected.
15. Eyesight
a. Von Graefe’s sign: lig lag SIGNS AND SYMPTOMS
b. Joffroy’s sign: absence of wrinkling of forehead on looking up 1. Large goiter with or without tracheal compression
c. Stellwag’s sign: decreased frequency of blinking 2. Goiter is nodular or lobulated, often palpable
d. Dalrimple’s sign: lid retraction exposing the upper sclera 3. Large goiter causes mediastinal compression with stridor,
e. Mobius sign: absence of convergence dysphagia and obstruction of superior vena cava
4. Hoarseness
DIAGNOSTIC EVALUATION
• Assessment measures in addition to palpation and auscultation MANAGEMENT
include thyroid function tests, such as laboratory measurement of • Small goiter: No treatment, annual review
thyroid hormones, thyroid scanning, biopsy, and ultrasonography.
• Large goiter: Partial thyroidectomy and radioactive iodine
• The most widely used tests are serum immunoassay for TSH and
• Recurrence is common after 10-20 years
free T4 (U.S. Preventive Services Task Force [USPSTF], 2015).
Free T4 levels correlate with metabolic status; they are elevated in
THYROID STORM
hyperthyroidism and decreased in hypothyroidism.
• Ultrasound, CT, and MRI may be used to clarify or confirm the • Rare but life-threatening sudden severe exacerbation of
results of other diagnostic studies. hyperthyroidism
• Other assessment measures include: • Causes: Precipitated by stress or infection with either unrecognized
1. T3 and T4 levels thyrotoxicosis or inadequately treated thyrotoxicosis; following
2. Thyroid uptake of radio-iodine subtotal thyroidectomy or radioactive iodine; trauma; pregnancy and
3. Presence of antibodies: TSH receptor antibody and anti- emotional stress
microsomal antibody
4. CT orbits thyroid scans HISTORICAL QUESTIONS IN THE EVALUATION OF THYROID
STORM
1. History of thyroid disease?
NURSING IMPLICATIONS
2. Symptoms of hyperthyroidism: tremor, agitation, weight loss,
• When thyroid tests are scheduled, it is necessary to determine if the nervousness, heat intolerance, proximal weakness, palpitations,
patient is allergic to iodine (shellfish) and whether the patient has and menstrual irregularity?
taken medications or agents that contain iodine, because these may 3. Thyroid manipulation?
alter the test results (Fischbach & Dunning, 2015). 4. Medication changes?
• Obvious sources of iodine containing medications include 5. Physiologic stressors: trauma, infections, exertion?
contrast agents and those used to treat thyroid disorders such as 6. Recent anesthesia?
radioactive iodine. 7. Recent iodinated contrast?
• Less obvious sources of iodine are topical antiseptics; 8. Infectious syndromes?
multivitamin preparations; food supplements that may contain
kelp and seaweed (frequently found in health food stores); and SIGNS AND SYMPTOMS
amiodarone (Cordarone), an antiarrhythmic agent (Surks,
1. Elevation of temperature
2016b).
2. Increase in heart rate
• Other medications that may affect test results are estrogens, 3. Irritable
salicylates, amphetamines, chemotherapeutic agents, 4. Delirius or comatose
antibiotics, corticosteroids, and diuretics. 5. Hypotension
• This information should be documented in the patient’s medical 6. Vomiting
record and the laboratory requisition. 7. Diarrhea

MANAGEMENT MANAGEMENT
• Immediate control: Propranolol 40mg/6hr orally Treatment started immediately with:
• Long-term control of the following: • Propranolol 80mg/6hrs orally (dose of 1-5mg/6hrs given IV)
1. Antithyroid drugs: Carbimazole 15mg tid initially and then • Potassium iodine 60mg daily orally/sodium iopodate 500mg daily
reducing it to 5mg tid for 12-18 months orally
2. Radioiodine ablation: Indicated for postmenopausal women • Carbimazole 60-120mg daily
and elderly men, used in recurrence following surgery and
• Dexamethasone 2mg/6hrs IV
given to fertile women, conception postponed to 1 year
• Fluid replacement
3. Surgery: Indicated with the presence of large goiter and poor
drug compliance • Antibiotics
4. Exophthalmus treatment: Corticosteroids, tarsorrhaphy, and
orbital decompression Emergency management in dental office:
5. Cardiac arrythmia treatment: Beta-blockers and if in • Terminate all treatment
euthyroid state, cardioversion may be done. • Have someone summon medical assistance
• Administer oxygen
MULTINODULAR GOITER • Monitor all vital signs
• Hyperthyroidism caused by multiple thyroid nodules is termed toxic • Initiate basic life support if necessary
multinodular goiter. • Start IV line with drip of crystalloid solution (150ml/hr)
• The nodules may be enlarged thyroid tissues or benign tumors • Transport patient to emergency care facility
(adenomas). These patients usually have had a goiter for years.
• The manifestations are milder than those seen in Graves' disease,
and the patient does not have exophthalmos or pretibial myxedema.
• Hyperthyroidism also can be caused by excessive use of thyroid
replacement hormones. This type of problem is called exogenous
hyperthyroidism.
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 HYPOTHYROIDISM • Causes: Congenital developmental defects, radioiodine, surgery,
• Hypothyroidism results from suboptimal levels of thyroid hormone. post-radiation, iodine deficiency, drug induced, Hashimoto’s
• Thyroid deficiency can affect all body functions and can range from thyroiditis, and recurrent hypothyroidism
mild, subclinical forms to myxedema (severe deficiency discussed
later), an advanced life-threatening form (Ross, 2016a). SIGNS AND SYMPTOMS
• The most common cause of hypothyroidism in adults is 1. Dry, cool, mottled skin, hoarse cry, broad flat nose, puffy face
autoimmune thyroiditis (Hashimoto disease), in which the 2. Protuberant abdomen, umbilical hernia and hypotonia
immune system attacks the thyroid gland. 3. Large posterior fontanelle
• Symptoms of hyperthyroidism may later be followed by those of 4. Lethargy, delayed stooling, and poor feeding or sucking
hypothyroidism and myxedema. 5. Cold to touch
• Hypothyroidism also commonly occurs in patients with previous 6. Delayed dentition
hyperthyroidism that has been treated with radioiodine or 7. Mental retardation
antithyroid medications or thyroidectomy (surgical removal of all
or part of the thyroid gland). In addition, there is an increased MANAGEMENT
incidence of thyroid cancer in men who have undergone radiation 1. Investigation: Cord blood T4, TSH, serum T4, RAIU (radioactive
therapy for head and neck cancer. Therefore, testing of thyroid iodine uptake), and x-ray of knee, foot and skull
function is recommended for all patients who receive such 2. Treatment: Medication include levothyroxine (initial dose of 10-
treatment. 15mcg/kg/dL), diet should include iodine-rich foods and there
• Insufficiency synthesis of thyroid hormones should be frequent follow-up checkups
• Female to male ratio is 6:1
• Causes: Hashimoto’s thyroiditis, thyroid failure following radio MYXEDEMA
iodine, surgical treatment of thyrotoxicosis, and drugs like • Severe hypothyroidism in which there is accumulation of hydrophilic
carbimazole, amiadarone, and iodine deficiency mucopolysaccharides in the skin and other tissues
• Primary hypothyroidism: thyroid cannot produce amount of • Common in women
hormone pituitary calls for • Two variants: hyperthyroid myxedema and hypothyroid myxedema
• Secondary hypothyroidism: thyroid isn’t being stimulated by • Cause: Increased deposition of glycosamine glycans and
pituitary to produce hormones Hashimoto’s thyroiditis

SIGNS AND SYMPTOMS MYXEDEMA COMA

1. Depression • Uncommon but life-threatening form of untreated hypothyroidism
2. Forgetfulness with physiological decompensation
3. Loss of eyebrow hair • Occurs in patients with long-standing hypothyroidism
4. Dry coarse hair • Precipitated by a climate induced hypothermia, infection, drug
5. Puffy face therapy and other systemic conditions
6. Enlarged thyroid (goiter)
7. Slow heartbeat SIGNS AND SYMPTOMS
8. Weight gain
1. Lethargy
9. Dry skin
2. Stupor
10. Constipation
3. Delirium
11. Arthritis
4. Hypotension
12. Brittle nails
5. Convulsions
13. Heavy menstrual period
6. Hypoglycemia
14. Infertility
7. Hyponatremia
8. Hypoventilation
HASHIMOTO’S THYROIDITIS 9. Coma
• Primary condition of hypothyroidism
• Autoimmune disease INVESTIGATIONS
• Described by Hakaru Hashimoto 1. Free T4 and TSH
2. T3 and T4 levels are decreased and TSH are elevated or normal
SIGNS AND SYMPTOMS 3. Serum electrolyte and serum osmolality
1. Weight gain 4. Serum creatinine
2. Enlarged thyroid gland 5. Serum glucose
3. Depression 6. Differential blood count
4. Sensitivity to heat and cold 7. Pan culture for sepsis
5. Fatigue
6. Hypoglycemia TREATMENT
7. Increased cholesterol level 1. Hyperventilation if respiratory acidosis is significant
2. Immediate IV levothyroxine given
DIAGNOSIS 3. Loading dose of 500-800mcg followed by 50-100mcg daily
1. T3 and T4 levels 4. Hydrocortisone 5-10mg/hr
2. Presence of TPO (thyroid peroxidase) antibodies 5. Treatment of associated infection
3. Positive ANF or antinuclear antibodies 6. Correction of hyponatremia with saline
7. Correction of hypoglycemia with IV dextrose
TREATMENT
1. Thyroxine therapy
2. Levothyroxine: Helps in both hypothyroidism and goiter shrinkage

CRETINISM
• Hypothyroidism dating from birth
• Tyroxine is essential for growth and development of brain during
the first three years
• Earlier onset greater is the brain damage

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 THYROID TESTS
• T3, T4 and TSH levels
• Presence of TPO antibodies
• Thyroid scan
• Thyroid uptake test
THYROIDECTOMY
• Surgical removal of all or a part of the gland
• Indications: Thyroid carcinoma, hyperthyroidism, very enlarged
thyroid and symptomatic obstruction
COMPLICATIONS
1. Hypothyroidism
2. Laryngeal nerve injury
3. Hypoparathyroidism
4. Infection
5. Chyle leak
6. Surgical scar
PARATHYROID DISORDERS
HYPERPARATHYROIDISM
PATHOPHYSIOLOGY
• The parathyroid glands maintain calcium and phosphate balance.
Serum calcium level is normally maintained within a narrow range.
• Increased levels of parathyroid hormone (PTH) act directly on the
kidney, causing increased kidney reabsorption of calcium and
increased phosphorus excretion. In hyperparathyroidism, these
processes cause hypercalcemia (excessive calcium) and
hypophosphatemia (inadequate blood phosphorus level).
• In bone, excessive PTH levels increase bone resorption (bone loss
of calcium) by decreasing osteoblastic (bone production) activity
and increasing osteoclastic (bone destruction) activity. This
process releases calcium and phosphorus into the blood and
reduces bone density.
• With chronic calcium excess and hypercalcemia, calcium is
deposited in soft tissues. Although the exact triggering mechanisms
are unknown, primary hyperparathyroidism results when one or
more parathyroid glands do not respond to the normal feedback of
serum calcium levels. The most common cause is a benign tumor
in one parathyroid gland.
ASSESSMENT
• Manifestations of hyperparathyroidism may be related either to the
effects of excessive PTH or to the effects of the accompanying
hypercalcemia.
- Ask about any bone fractures, recent weight loss, arthritis, or
psychological stress.
- Ask whether the patient has received radiation treatment to the
head or neck.
- The patient with chronic disease may have a waxy pallor of the
skin and bone deformities in the extremities and back.
MANAGEMENT
• Priority nursing interventions focus on monitoring and preventing
injury
• Drugs: Uritol, cinacalcet (Sensipar), IV phosphates
• Surgical management: parathyroidectomy
HYPOPARATHYROIDISM
• Hypoparathyroidism is a rare endocrine disorder in which
parathyroid function is decreased. Problems are directly related to
a lack of parathyroid hormone (PTH) secretion or to decreased
effectiveness of PTH on target tissue. Whether the problem is a lack
of PTH secretion or an ineffectiveness of PTH on tissues, the result
is the same: hypocalcemia.
• Iatrogenic hypoparathyroidism, the most common form, is
caused by the removal of all parathyroid tissue during total
thyroidectomy or by surgical removal of the parathyroid glands.
• Idiopathic hypoparathyroidism can occur spontaneously. The
exact cause is unknown, but an autoimmune basis is suspected. It
may occur with other autoimmune disorders such as adrenal
insufficiency, hypothyroidism, diabetes mellitus, pernicious
anemia, and vitiligo.
• Hypomagnesemia (decreased serum magnesium levels) may also
cause hypoparathyroidism. Hypomagnesemia is seen in patients
with malabsorption syndromes, chronic kidney disease, and
malnutrition. It causes impairment of PTH secretion and may
interfere with the effects of PTH on the bones, kidneys, and calcium
regulation.
ASSESSMENT
• Ask about any head or neck surgery or radiation therapy
because these treatments may damage the parathyroid glands and
cause hypoparathyroidism.
• Also ask whether the neck has ever sustained a serious injury in
a car crash or by strangulation.
• Assess whether the patient has any manifestations of
hypoparathyroidism, which may range from mild tingling and
numbness to muscle tetany. Tingling and numbness around the
mouth or in the hands and feet reflect mild to moderate
hypocalcemia. Severe muscle cramps, spasms of the hands and
feet, and seizures (with no loss of consciousness or incontinence)
reflect a more severe hypocalcemia. The patient or family may
notice mental changes ranging from irritability to psychosis.
• The physical assessment may show excessive or inappropriate
muscle contractions that cause finger, hand, and elbow flexion. This
can signal an impending attack of tetany. Check for Chvostek's
sign and Trousseau's sign; positive responses indicate potential
tetany. Bands or pits may encircle the crowns of the teeth, which
indicate a loss of calcium from the teeth with enamel loss.
DIAGNOSTIC TESTS
• Diagnostic tests for hypoparathyroidism include
electroencephalography (EEG), blood tests, and CT scans.
EEG changes revert to normal with correction of hypocalcemia.
Serum calcium, phosphorus, magnesium, vitamin D, and urine
cyclic adenosine monophosphate (cAMP) levels may be used in
the diagnostic workup for hypoparathyroidism. The CT scan can
show brain calcifications, which indicate chronic hypocalcemia.
INTERVENTION
• Nonsurgical management of hypoparathyroidism focuses on
correcting hypocalcemia, vitamin D deficiency, and
hypomagnesemia. For patients with acute and severe
hypocalcemia, IV calcium is given as a 10% solution of calcium
chloride or calcium gluconate over 10 to 15 minutes. Acute vitamin
D deficiency is treated with oral calcitriol (Rocaltrol), 0.5 to 2 mg
daily. Acute hypomagnesemia is corrected with 50% magnesium
sulfate in 2-mL doses (up to 4 g daily) IV. Long-term oral therapy
for hypocalcemia involves the intake of calcium, 0.5 to 2 g daily, in
divided doses.
• Long-term therapy for vitamin D deficiency is 50,000 to 400,000
units of oral ergocalciferol daily. The dosage is adjusted to keep the
patient's calcium level in the low-normal range (slightly
hypocalcemic), enough to prevent symptoms of hypocalcemia. It
must also be low enough to prevent increased urine calcium levels,
which can lead to stone formation.
• Nursing management includes teaching about the drug regimen and
interventions to reduce anxiety. Teach the patient to eat foods high
in calcium but low in phosphorus. Milk, yogurt, and processed
cheeses are avoided because of their high phosphorus content.
Stress that therapy for hypocalcemia is lifelong. Advise the patient
to wear a medical alert bracelet. With adherence to the prescribed
drug and diet regimen, the calcium level usually remains high
enough to prevent a hypocalcemic crisis.