Transcript Interventions for Clients with Problems of the Thyroid and

Interventions for Clients
with Problems of the Thyroid
and Parathyroid Glands
 Hormones from the thyroid and parathyroid
glands affect general metabolism,
electrolyte balance, and excitable
membrane activity.
 Therefore a disturbance in either thyroid or
parathyroid function usually has widespread
clinical manifestations.
 With mild disturbances, the problems are
subtle.
 With more severe disturbances, the
problems may be life threatening
Hyperthyroidism
 Excessive thyroid hormone secretion results
in hyperthyroidism.
 The clinical manifestations of
hyperthyroidism are referred to as
thyrotoxicosis.
 Thyroid hormones affect all metabolic
processes in all body organs and therefore
produce numerous and varied clinical
manifestations.
 Hyperthyroidism can be temporary or
permanent depending on the cause
Hyperthyroidism
 Because thyroid hormones stimulate most body
systems, excessive thyroid hormones produce a state
of hypermetabolism with increased sympathetic
nervous system activity
 Thyroid hormones directly stimulate the heart. The
increased heart rate and stroke volume in
hyperthyroidism cause an increase in cardiac output
and peripheral blood flow.
 This excessive or hyperdynamic circulatory state
results from an increase in the number of adrenergic
receptors on the heart muscle
Hyperthyroidism
 Elevated levels of thyroid hormones affect protein,
carbohydrate, and lipid metabolism.
 Protein synthesis (buildup) and degradation
(breakdown) are increased. Breakdown exceeds
buildup, causing a net loss of protein known as a
negative nitrogen balance. Glucose tolerance is
decreased, and the client has hyperglycemia
(elevated blood glucose levels).
 Fat metabolism is increased, which results in
decreased body fat stores. Although the client has an
increased appetite, food intake does not meet energy
demands, and the client loses weight. With prolonged
hyperthyroidism, the client is in a state of chronic
nutritional deficiency
Hyperthyroidism
 If hyperthyroidism is present before
puberty, sexual development is delayed.
 If hyperthyroidism develops after puberty,
women experience menstrual irregularities
and decreased fertility.
 Both men and women with hyperthyroidism
experience an increased libido (sexual
urge or interest)
Hyperthyroidism
Hyperthyroidism
Hyperthyroidism
 Age, gender, and usual weight are recorded.
 The client may report a recent weight loss and an
increased appetite.
 Diarrhea is common.
 A hallmark of hyperthyroidism is heat intolerance. The
client may have diaphoresis (increased sweating)
even when environmental temperatures are
comfortable for others. The client often wears lighter
clothing in cold weather.
 The client may also report palpitations or chest pain
as a result of the cardiovascular effects.
 The nurse asks about changes in breathing patterns,
because dyspnea (with or without exertion) is
common
Hyperthyroidism
 Visual changes may be the earliest problem noted
in the client with hyperthyroidism, especially
ophthalmopathy with Graves' disease.
 The client is asked about changes in vision, such as
blurring or double vision and tiring of the eyes
 Fatigue, weakness, and insomnia are common.
 Family and friends may report that the client has
become more irritable or depressed
 Women are asked about changes in menses,
because amenorrhea or a decreased menstrual flow
is common
Hyperthyroidism. Assessment
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Two types of ophthalmopathy (abnormal eye appearance or
function) are common with hyperthyroidism: eyelid retraction
(eyelid lag) and globe (eyeball) lag.
In eyelid lag, which occurs in all forms of thyrotoxicosis, the upper
eyelid fails to descend when the client gazes slowly downward.
In globe lag, the upper eyelid pulls back faster than the eyeball
when the client gazes upward
Infiltrative ophthalmopathy, which leads to exophthalmos, is
common in clients with Graves' disease.
The wide-eyed or "startled" look is due to edema in the extraocular
muscles and increased fatty tissue behind the eye, which pushes
the globe forward. Pressure on the optic nerve may impair vision.
Swelling and shortening of the muscles may cause problems with
focusing. If the eyelid fails to close completely and the eye is
unprotected, the eye may become overdry and prone to corneal
ulceration or infection.
The nurse observes the client's eyes for excessive tearing and a
bloodshot appearance and asks about sensitivity to light
(photophobia)
Hyperthyroidism. Assessment
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The nurse palpates the thyroid gland to determine the
presence of a mass or general enlargement, observing the
size and symmetry of the gland. In goiter, a generalized
thyroid enlargement in people with Graves' disease, the
thyroid gland may increase to four times its normal size.
Bruits (turbulence from increased blood flow) may be heard
with a stethoscope.
The nurse inspects the client's hair and skin. Fine, soft, silky
hair and smooth, moist skin are common with
hyperthyroidism.
The client may have extremity muscle weakness,
hyperactive deep tendon reflexes, or tremors.
Gross motor movements are observed for tremors,
especially of the hands.
Reflexes may be hyperactive. The client may appear
extremely restless, irritable, and fatigued
Hyperthyroidism. Assessment
 The client with hyperthyroidism often experiences
emotional lability (mood instability), irritability,
decreased attention span, and manic behavior.
 Mild to severe hyperactivity often leads to a state of
fatigue because of the inability to sleep well.
 The nurse asks the client whether he or she has been
crying or laughing inappropriately or has had difficulty
concentrating.
 The client's family members or significant other often
report these changes in mental or emotional status
Hyperthyroidism. Assessment
Hyperthyroidism. Assessment
 Thyroid scan
 Ultrasonography
 Electrocardiography
Hyperthyroidism. Interventions
 The cardiac problems of hyperthyroidism
include increased systolic blood pressure, a
widened pulse pressure, tachycardia, and
other dysrhythmias.
 The goals of nonsurgical management are
to decrease the effect of thyroid hormone
on cardiac function and to reduce thyroid
hormone secretion.
 Surgery may be necessary when
nonsurgical interventions are unsuccessful
Hyperthyroidism. Interventions
Nonsurgical management
 The nurse monitors the client's apical pulse, blood
pressure, and temperature at least every 4 hours. The
client is instructed to report any palpitations,
dyspnea, vertigo, or chest pain immediately.
 Fatigue is common, and the client is encouraged to
rest. The environment is kept as quiet as possible.
 Frequent bed linen changes, sponge baths, and a cool
environment decrease discomfort caused by
diaphoresis and heat intolerance
Hyperthyroidism. Interventions
Hyperthyroidism. Interventions
 Radioactive iodine (RAI) therapy is
contraindicated in pregnant women
because 131I crosses the placenta and
can adversely affect the fetal thyroid
gland
Hyperthyroidism. Interventions
Surgical management
 Antithyroid drugs and RAI therapy are now the most
common treatments for clients with hyperthyroidism.
 Surgery to remove all or part of the thyroid gland may
be necessary for clients who have a large goiter
causing tracheal or esophageal compression or who
are unresponsive to antithyroid drugs.
 Removal of all (total thyroidectomy) or part (subtotal
thyroidectomy) of the thyroid tissue decreases the
production of thyroid hormones.
 Clients undergoing a total thyroidectomy must take
lifelong thyroid hormone replacement.
 This surgery is also indicated in certain types of
thyroid cancer
Hypothyroidism
Hypothyroidism
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Cellular energy production is decreased, and many
metabolites build up.
The metabolites are compounds of proteins and sugars
called glycosaminoglycans.
These compounds build up inside cells, which increases the
mucous and water, forms cellular edema, and changes
organ texture. The cellular edema is mucinous edema
(called myxedema) rather than edema caused by water
alone.
This edema changes the appearance of the client with fullblown hypothyroidism. Nonpitting edema forms everywhere
and is especially evident around the eyes, in the hands and
feet, and between the shoulder blades.
These same compounds cause the tongue to thicken and
edema to form in the larynx, making the voice more husky.
It is likely that these metabolites build up in other tissues
and organs, decreasing general physiologic function
Hypothyroidism
 Myxedema coma is a rare but serious complication
of untreated or inadequately treated hypothyroidism.
The decrease in metabolism in cardiac tissue causes
the heart muscle to become flabby and the chamber
size to increase.
 The result is decreased cardiac output and decreased
perfusion to the brain and other vital organs.
 The decreased perfusion makes the already slowed
cellular metabolism worse, resulting in tissue and
organ failure.
 The mortality rate for myxedema coma is extremely
high, and this condition is considered a lifethreatening emergency
Hypothyroidism
Causes of mixedema coma
Hypothyroidism
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HISTORY
A decrease in thyroid hormone produces a variety of signs
and symptoms related to decreased metabolic activity.
The client often reports an increase in time spent sleeping,
sometimes up to 14 to 16 hr/day. The client may also have
generalized weakness, anorexia, muscle aches, and
paresthesias.
Constipation is common.
The client often has cold intolerance, and the nurse asks if
more blankets at night or sweaters and extra clothing in
warm weather have been needed.
Both male and female clients may identify a decrease in
libido. In addition, women with hypothyroidism may have
had difficulty becoming pregnant or experienced changes in
menses (heavy, prolonged bleeding or amenorrhea).
Men can have problems with impotence and fertility
Hypothyroidism
 The client is asked about his or her current
or previous use of medications, such as
lithium, aminoglutethimide, sodium or
potassium perchlorate, thiocyanates, or
cobalt. All of these drugs can impair the
production of thyroid hormone.
 The client is asked whether he or she is
taking any tranquilizers or opioids
(hypothyroidism increases the sensitivity to
these drugs as a result of decreased
metabolism)
Hypothyroidism
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MYXEDEMA COMA
The following problems are
associated with this condition:
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Coma
Respiratory failure
Hypotension
Hyponatremia
Hypothermia
Hypoglycemia
Untreated myxedema coma leads
to shock, organ damage, and
death.
The nurse assesses the client with
hypothyroidism every shift for
changes that indicate increasing
severity of hypothyroid symptoms,
especially changes in mental
status.
Hyperparathyroidism
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The parathyroid glands maintain calcium and phosphate
balance.
Increased levels of parathyroid hormone (PTH) act directly
on the kidney, causing increased kidney reabsorption of
calcium and increased phosphate excretion.
These processes cause hypercalcemia (excessive calcium)
and hypophosphatemia (inadequate phosphate) in the
client with hyperparathyroidism.
In the 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
phosphate into the circulation and demineralizes bone.
When the normal solubility of calcium in the serum is
exceeded, as in long-standing hypercalcemia, calcium is
deposited in soft tissues
Hyperparathyroidism
Assessment
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The nurse asks about the client's symptoms and any bone fractures, recent
weight loss, arthritis, or psychologic distress.
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Any history of radiation treatment to the head or neck is also obtained. The
client with long-standing disease may have a waxy pallor of the skin and
bone deformities in the extremities and back.
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The clinical features of hyperparathyroidism may be related either to the
effects of excessive PTH or to the effects of the accompanying
hypercalcemia.
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High levels of PTH cause renal calculi (kidney stones) and nephrocalcinosis
(deposits of calcium in the soft tissue of the kidney).
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Bone lesions are due to an increased rate of bone destruction and result in
pathologic fractures, bone cysts, and osteoporosis in advanced cases.
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Gastrointestinal manifestations (e.g., anorexia, nausea, vomiting, epigastric
pain, constipation, and weight loss) are common, particularly when serum
calcium levels are high. Hypergastrinemia (elevated serum gastrin levels) is
caused by hypercalcemia and leads to peptic ulcer disease.
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Fatigue and lethargy may be present and become more severe as the
serum calcium levels increase. When serum calcium levels are greater than
12 mg/dL, the client may have psychosis with mental confusion, which
leads to coma and death if left untreated
Hyperparathyroidism
 Serum PTH, calcium, and phosphate levels and urine
cyclic adenosine monophosphate (cAMP) are the most
commonly used laboratory tests to detect
hyperparathyroidism
 X-rays may show kidney stones, calcium deposits, and
bone lesions, such as cysts or fractures. Generalized
bone demineralization and resorption in the long
bones occur in the client with chronic
hyperparathyroidism.
 Other diagnostic tests include arteriography,
computed tomography (CT), venous catheterization of
the thyroid veins with sampling of the blood for PTH
levels, and ultrasonography.
 The nurse explains the procedures and cares for the
client undergoing diagnostic tests
Hyperparathyroidism
Interventions
 Nonsurgical management
 Diuretic and fluid therapy.
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The most common therapy for reducing serum calcium levels
in clients who are not candidates for surgery is hydration and
furosemide, a diuretic that increases kidney excretion of
calcium.
IV saline in large volumes also promotes renal calcium
excretion.
The nurse monitors cardiac function and intake and output
every 2 to 4 hours during hydration therapy. Continuous
cardiac monitoring may be required.
The nurse closely monitors serum calcium levels and
immediately reports any precipitous drop to the physician.
Sudden drops in calcium levels may cause tingling and
numbness in the muscle
Hyperparathyroidism
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Drug therapy.
When hydration and furosemide cannot reduce
hypercalcemia, or if it becomes necessary to discontinue IV
fluids, additional medications can help to reduce the clinical
manifestations of hyperparathyroidism, especially those
related to hypercalcemia.
Phosphates. Oral phosphates inhibit bone resorption and
interfere with calcium absorption. IV phosphates are used
only when serum calcium levels must be lowered rapidly.
Calcitonin. Calcitonin decreases skeletal calcium release and
increases the kidney excretion of calcium. Calcitonin is not
effective when used alone because of its short duration of
action. Its therapeutic effects are greatly enhanced if given
in conjunction with glucocorticoids
Hyperparathyroidism
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Calcium Chelators. Some drugs lower calcium levels by binding
(chelating) calcium, which reduces the levels of free calcium.
Mithramycin, a cytotoxic agent, is the most effective and
potent calcium chelator used to lower serum calcium levels.
In most clients a single IV dose of 10 to 15 mg/kg of body
weight by slow infusion can lower serum calcium levels within
48 hours. However, the toxic effects limit its use to two or
three doses. Thrombocytopenia (decreased circulating platelets
and an increased tendency to bleed) and kidney and liver
toxicity can result after only one dose. Liver function studies,
blood urea nitrogen and creatinine, complete blood count
(CBC), and serum calcium levels are closely monitored in the
client receiving mithramycin. Another calcium chelator is
penicillamine (Cuprimine, Pendramine)
Surgical management. Surgical management of
hyperparathyroidism involves a parathyroidectomy
Hypoparathyroidism
 Hypoparathyroidism is an uncommon 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 deliberate
surgical removal of the parathyroid glands.
Hypoparathyroidism
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Idiopathic hypoparathyroidism is a rare condition that can
occur spontaneously. The exact cause is unknown, but an
autoimmune basis is suspected because antiparathyroid
antibodies are present in many affected clients. In addition,
hypoparathyroidism is often associated with the following
autoimmune disorders: adrenal insufficiency,
hypothyroidism, diabetes mellitus, pernicious anemia,
gonadal failure, and vitiligo.
Hypomagnesemia (decreased serum magnesium levels)
may also cause hypoparathyroidism. Hypomagnesemia is
seen in alcoholics and in clients with malabsorption
syndromes, chronic renal disease, and malnutrition. It
causes impairment of PTH secretion and may interfere with
PTH effects on the bones and kidneys
Hypoparathyroidism
Assessment
 The nurse begins assessment of the client with
suspected hypoparathyroidism by asking about any
head or neck surgery or radiation therapy, because
these treatments may cause hypoparathyroidism.
 The client is asked about the signs and symptoms of
hypoparathyroidism, which may range from mild
tingling and numbness to tetany. Tingling and
numbness around the mouth or in the hands and feet
reflect mild to moderate hypocalcemia. Severe muscle
cramps, carpopedal spasms, and seizures (with no
loss of consciousness or incontinence) reflect a more
severe hypocalcemia. The client or caregiver may
notice mental changes ranging from irritability to
psychosis
Hypoparathyroidism
 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.
 The nurse checks for Chvostek's sign and Trousseau's
sign; positive responses indicate potential tetany.
 A parkinsonian-like syndrome may be evident.
 The presence of cataracts denotes chronic
hypocalcemia.
 Bands or pits may encircle the crowns of the teeth,
which indicates a loss of calcium from the teeth and
causes enamel loss. The roots of the client's teeth
may be defective
Hypoparathyroidism
 Diagnostic tests for hypoparathyroidism include
electroencephalography (EEG), blood tests, and
computed tomography (CT).
 EEG changes are nonspecific and revert to normal
with correction of hypocalcemia. Serum calcium,
phosphate, 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
Hypoparathyroidism
Interventions
 Management of hypoparathyroidism focuses on correcting
hypocalcemia, vitamin D deficiency, and hypomagnesemia.
 For clients with acute and severe hypocalcemia, IV calcium is
administered as a 10% solution of calcium chloride or calcium
gluconate over 10 to 15 minutes.
 Acute vitamin D deficiency is treated with calcitriol (Rocaltrol), 0.5
to 2.0 mg/day.
 Acute hypomagnesemia is corrected with 50% magnesium sulfate
in 2-mL doses (up to 4 g/day) either intramuscularly or
intravenously.
 Long-term oral therapy for hypocalcemia involves the
administration of calcium, 0.5 to 2.0 g/day in divided doses.
 Long-term therapy for vitamin D deficiency is 50,000 to 400,000
units of ergocalciferol daily. The dosage is adjusted to keep the
client'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
concentrations, which can lead to stone formation
Hypoparathyroidism
 Nursing management includes teaching about the
medication regimen and interventions to reduce
anxiety.
 The client is instructed to eat foods high in calcium
but low in phosphorus.
 Milk, yogurt, and processed cheeses are avoided
because of their high phosphorus content.
 The nurse stresses that therapy for hypocalcemia is
lifelong. The client is advised to use some form of
identification, such as a Medic Alert bracelet or a
wallet card.
 With adherence to the prescribed drug and diet
regimen, the calcium level usually remains high
enough to prevent a hypocalcemic crisis