How Hyperthyroidism and Hypothyroidism affect our Body

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How Hyperthyroidism and Hypothyroidism …
Oyid: Tipping the scales: Understanding thyroid imbalances. 1
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Nursing Critical Care
Issue: Volume 8(1 ). january 2013, p 23-28
Copyright: © 2013 lippincott Will iams & Wilkins, Inc.
Publication Type: [Feature]
DOl: 10.1 097/01.CCN .0000418818.21604.22
ISSN: 1558·447X
Accession: 01244666·201301 000-00006
< Previous Article Table of Contents
Tipping the scales: Understanding thyroid imbalances
Crawford, Ann PhD, RN; Harris, Helene MSN, RN
Author Information
Next Article >
Ann Crawford is a professor in the College of Nursing at the University of Mary Hardin-Baylor in Belton, Tex.
Helene Harris is a clinical educator at Central Texas Veterans Health care System in Temple, Tex.
Find out how to recognize and respond to potentially life-threatening metabolic imbalances.
The authors have disclosed that they have no financial relationships related to this article.
Thyroid hormones affect overall metabolism and electrolyte balance. Alterations in
thyroid hormone function can cause widespread and potentially life-threatening
effects. This article reviews hyperthyroidism and hypothyroidism and what you need
to know about each condition. For details on this endocrine gland, see About the
thyroid.
~RTHYROID~
Figure. No
caption a …
Hyperthyroidism is the clinical syndrome that results when tissues are exposed to high levels of circulating
thyroid hormone. In most cases, hyperthyroidism is due to hyperactivity of the thyroid gland.1 This common
endocrine disorder can occur at any age, although patients typically are diagnosed between ages 20 and 40.
Women are much more likely to be diagnosed with a form of hyperthyroidism than men.2,3 The increased
levels of circulating thyroid hormones increase sympathetic nervous system activity and increase metabolic
rate, causing many of the clinical manifestations of hyperthyroidism.1
Thyroid hormone overstimulation on the cardiovascular system causes “fight-or-flight” types of responses,
including an increase in heart rate, stroke volume, myocardial contractility, and BP.1 ,2 No matter what the
cause, manifestations of overproduction of thyroid hormones are termed thyrotoxicosis. However,
thyrotoxicosis isn’t synonymous with hyperthyroidism and thyrotoxicosis can occur without hyperthyroidism.
For a list of the manifestations of hyperthyroidism, see Clinical manifestations of hyperthyroidism and
hypothyroidism.
Elevated thyroid hormone levels increase the body’s metabolic rate and affect the metabolism of proteins, fat s,
and carbohydrates. Because of th is, although the patient has an increased appetite and food intake, energy
needs exceed the supply and the person loses weight. With the high metabolic rate, protein degradation
exceeds protein synthesis, causing a negative nitrogen balance. Fat metabolism is increased, reducing fat
stores. Sustained hyperthyroidism leads to more chronic nutritional deficits.1 ,2 Hypersecretion of thyroid
hormones can also affect the secretion of other endocrine hormones within the hypothalamus and anterior
pituitary gland, including sex hormone production.2
Thyrotoxicosis may also be caused by radiation exposure, ingestion of excess thyroid hormone, thyroiditis
(usually temporary), interferon-alpha therapy, pituitary tumors, and metastatic thyroid cancer. Patients taking
the antiarrhythmic drug amiodarone, a heavily iodinated compound, can develop hyperthyroidism or
hypothyroidism.3 Hyperthyroidism may be acute or chronic, depending on its underlying etiology.
Graves disease is an autoimmune disease, characterized by abnormal stimulation of the thyroid gland, in which
the body makes antibodies that bind to the thyro id-stimulation hormone (TSH) receptor sites in the thyroid.
Thyroid-stimulating immunoglobulins (TS is) attach to the thyroid tissue, causing gland hypertrophy and thyroid
hormone overproduction. Patients with Graves disease will demonstrate the key features of thyrotoxicosis.1 ,3
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Outline
HYPERTHYROIDISM
Diagnostic testing and
management
Nursing considerations and
patient teaching
HYPOTHYROIDISM
Diagnostic testing and
management
Nursing interventions
Patient education
Staying in balance
About the thyroid ..
Serious trouble
REFERENCES:
IMAGE GALLERY
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Ovid: Tipping the scales: Understanding thyroid imbalances.
Back to Top
Toxic multinodulor goiter is hyperthyroidism caused by multiple thyroid nodules. usually composed of enlarged
thyroid tissue or benign tumors. The overproduction of thyroid hormones is usually less severe than in Graves
disease, and the clinical presentation wilt be similar, though without the manifestation of exophthalmos or
pretibial edema.2
Diagnostic testing and management — Table Clinical man if…
Hyperthyroidism is diagnosed based on patient history, clinical presentation, and thyroid hormone lab studies,
and including T3, T4, TSH, and T3 resin uptake (T3RU). In addition, measurement ofTSH receptor antibodies
(TSH-RAb) may be used to diagnose Graves disease.2
A radioiodine uptake and thyroid scan may be performed to evaluate the thyroid gland’s size, position, and
function. A thyroid ultrasound may also be used to determine the size of the thyroid gland and presence of
masses or nodules.2,4
Treatment for hyperthyroidism includes antithyroid drug therapy, radioiodine, and surgery (subtotal or neartotal
thyroidectomy).S Medications such as methimazole and propylthiouracil (PTU) inhibit the synthesis of
thyroid hormones, but don’t inactivate circulating thyroid hormones or those stored in the thyroid. These
medications are used for long-term management. Potassium iodide and iodine solutions inhibit the synthesis
and the release of the thyroid hormone, and generally are used for short-term therapy, such as before thyroid
surgery.6 Beta-blockers can be used to help control adrenergic signs and symptoms, especially in the early
stages of treatment before the antithyroid drugs take effect. Beta-blockers block the effects of the thyroid
hormone on the sympathetic receptors of the heart, decreasing myocardial oxygen demands.6
Radioiodine (radioactive iodine) causes progressive destruction of thyroid cells . Potential adverse effects
include pharyngitis or neck tenderness for a few days, and complications include hypothyroidism.6 Radioiodine
may exacerbate the ophthalmopathy for patients with Graves disease (more on this later).6 Because fewer
than 50% of patients treated with antithyroid medications remain in long-term remission, radioactive iodine is
used increasingly as a permanent treatmentS
Back to Top
Surgery, once a primary method of treating hyperthyroidism, is reserved today for patients with special
circumstances, such as inability to take antithyroid medication, pregnancy, a large goiter, or
ophthalmopathy.2,5 Most of the thyroid gland is removed, permanently reducing thyroid hormone production.
Following the surgery, patients usually must take thyroid replacement medication daily to prevent
hypothyroidism.5,7 Major complications of surgery include bleeding, laryngeal edema, hypoparathyroidism,
and recurrent laryngeal nerve damage.8
Nursing considerations and patient teaching
Monitor the patient’s vital signs closely; an alteration in metabolic rate can lead to significant increases in heart
rate, BP, and temperature. Assess all body systems and monitor food intake, appetite, and weight. Assess
muscle strength and watch for tremors, heat intolerance, emotional changes, and irritability, which could
indicate thyrotoxicosis. Assess and document intake and output.
Monitor the patient’s thyroid hormone levels (to determine if antithyroid medications are effective, and to
monitor for increasing symptomology), as welt as liver function tests. Some antithyroid drugs can cause
leukopenia, agranulocytosis, and other hematologic dysfunction, so monitor the patient’s complete blood celt
count and lactate dehydrogenase. Closely monitor serum glucose and electrolyte levels, especially in patients
exhibiting manifestations of thyrotoxic crisis (for more on thyrotoxic crisis, see Serious trouble).6
Iodine toxicity can occur if the patient is taking too much iodine or the dose is too high. Signs of iodine toxicity
include burning sensation in the mouth and throat, metallic taste in the mouth, sore teeth and gums, increased
salivation, nasal discharge, gastrointestinal upset, and periorbital edema. Teach patients to report these
symptoms to their hea lthca re provider immediately. Because antithyroid medications work to decrease thyroid
function, be alert for manifestations of hypothyroidism.6 Consult the full prescribing information for details
about drugs your patient is prescribed.
Encourage patients to have regular follow-up appointments, which wilt include monitoring their thyroid
hormone levels. Teach them to avoid foods high in iodine, such as seafood, tofu, soy, cheddar cheese,
mayonnaise, and iodized salt, and to wear a medical-alert bracelet or medal.
Back to Top
Patients with Graves disease are at risk for Graves ophthalmopathy, an autoimmune disease in which
inflammation increases the volume of the extraocular muscles and retro-orbital tissues. Te ll patients to notify
their healthcare provider if they develop eye swelling or irritation, blurred vision. and excessive tearing
worsened by exposure to cold, wind, or bright lights.9
2
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Ovid: Tipping the scales: Understanding thyroid imbalances.
~ A deficiency of thyroid hormones, hypothyroidism causes a decreased metabolic ra te. Primary hypothyroidism
(99% of diagnosed cases) is caused by autoimmune, disease, or iatrogenic destruction of the thyroid gland.
~ Iatrogenic causes include surgical removal or irradiation of thyroid tissue, or medications that suppress thyroid
function, such as antithyroid drugs and lithium. Other causes include postpartum thyroiditis, subacute
granulomatous thyroiditis, and inadequate ingestion of necessary ingredients for thyroid hormone formation
(such as iodine or tyrosine).2, 10 Amiodarone, as mentioned earlier, can cause hyperthyroidism or
hypothyroidism.3
Congenital hypothyroidism occurs in about 1 of every 5,000 births, and is a preventable cause of mental
retardation. With proper neonatal screening and treatment, this problem is easily reso lved.1 In adults with
adequate iodine intake, the most common cause of hypothyroidism is chronic autoimmune thyroiditis, or
Hashimoto disease.7, 10
Less commonly, hypothyroidism is caused by decreased secretion of thyrotropin-releasing hormone (TRH)
from the hypothalamus or decreased secretion ofTSH from the anterior pituitary gland.11 Insufficient
stimulation of the thyroid gland by TSH (central hypothyroidism) is caused by either pituitary disease
(secondary hypothyroidism) or hypothalamic disease (tertiary hypothyroidism).11
Hypothyroidism occurs most often in women, and is usually diagnosed between the ages of 30 and 60 .2,7
Overall, hypothyroidism is more common than hyperthyroidism.12
In hypothyroidism, low circulating levels of thyroid hormone cause a generalized slowing of metabolic
processes. Low thyroid hormone levels stimulate the anterior pituitary gland to release TSH in an attempt to
trigger the production of more thyroid hormones. TSH binds to the thyroid tissue and over time causes goiter,
an abnormal enlargement of the thyroid gland, although it doesn’t necessarily promote increased thyroid
hormone production.1 ,2, 10 The low metabolic rate has an effect on most tissues and organs. As cellular energy
diminishes, metabolites (called glycosaminoglycans) build up within the cells, forming a cellular edema of water
mixed with mucus, known as myxedema. This non-pitting edema develops throughout the body, most
conspicuously around the eyes, in the hands and feet, and between the scapulae. The tongue appears
enlarged and the patient’s voice may sound husky or hoarse due to laryngeal edema.2
Back to Top
Clinical manifestations of hypothyroidism are caused by the decreased metabolic rate. Because
hypothyroidism often occurs slowly, the onset of signs and symptoms is insidious and develops over months to
years.2 Because many of the clinical manifestations are vague, nonspecific, and slow to develop, they may be
ignored or unnoticed by patients and their families .1,2,10
Diagnostic testing and management
As with hyperthyroidism, diagnosis for hypothyroidism is based on patient history, clinical manifestations, and
serum thyroid hormone levels and TSH. In overt primary hypothyroidism, serum TSH is elevated and T3 and T4
levels are decreased. In subclinical primary hypothyroidism, serum TSH levels are high and T3 and T4 levels are
normal.4, 10,11
The treatment of choice for hypothyroidism is thyroid hormone replacement with levothyroxine, a synthetic
form ofT4. Levothyroxi ne has the same effects as the body’s own thyroid hormone, increasing the metabolic
rate, which in turn increases the heart rate; respiratory rate; BP; and fat, protein, and carbohydrate
metabolism.6 Adverse reactions to levothyroxine are potentially serious and may mimic the manifestations of
hyperthyroidism.6
Use levothyroxine cautiously in older adults, and patients with cardiovascular disease, hypertension, or
diabetes. Patients with aspirin allergy, adrenal insufficiency, and severe cardiovascular disease shouldn’t take
levothyroxine .13
Back to Top
Other medications for treating hypothyroidism include desiccated thyroid extract (pork or beef), liothyronine
(T3), and liotrix (4:1 mixture ofT4 and T3).14
Nursing interventions
Obtain a health history and perform medication reconci liation, including all prescription and over-the-counter
medications, as well as herbal and nutritional supplements. Monitor vital signs regularly, and thoroughly
assess the patient’s physiologic status, including cardiovascular status, neurologic status, pulmonary status,
and renal function. To help determine nutritional status, ask patients what they’ve weighed in the past. Weigh
the patient; monitor appetite and food intake levels, as well as overall intake and output. Monitor serum
thyroid hormone levels, blood urea nitrogen and creatinine, and blood glucose, as well as prothrombin time
and international normalized ratio if the patient is on anticoagulants (levothyroxine can affect blood glucose
levels in patients with diabetes and can alter the effects of anticoagulants).
3
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Ovid: Tipping the scales: Understanding thyroid imbalances.
Monitor for continued signs of hypothyroidism that may indicate a need to increase the medication dosage,
and signs of hyperthyroidism that may indicate a need to decrease the dosage. Use appropriate patient safety
measures, and assist with ambulation and activities of daily living as needed.6
Back to Top
Myxedema coma is a rare, life-threatening emergency that occurs due to unrecognized, untreated, or
undertreated hypothyroidism, and is often seen in older adults (usually women) in the winter months. The
patient will exhibit a worsening of hypothyroidism signs and symptoms (hypothermia, bradycardia,
hypotension, hypoventilation, hyponatremia, hypoglycemia, and metabolic acidosis), deteriorating
neurologically to a comatose state.16 Diminished metabolism causes respiratory depression, cardiovascular
collapse, and shock. 2,4,7 Treatment of myxedema coma includes mechanical ventilation, thyroid replacement
therapy, fluid and vasopressor administration, passive rewarming, and I.V. dextrose. However, even with
aggressive treatment, mortality is high.2,4,7
Patient education
Teach patients that thyroid replacement therapy must be taken for life, and not to discontinue medication or
change brands or dosages without contacting their healthcare provider. Because thyroid medications can
cause insomnia if taken at night, they’re usually administered in the morning on an empty stomach. Because
iron and calcium supplements and antacids can decrease absorption of levothyroxine, patients shouldn’t take
these supplements or antacids within 4 hours of taking levothyroxine. Patients should follow up with their
healthcare provider regularly, including assessment of serum thyroid hormone levels.
Teach patients to change positions slowly and to notify their healthcare provider immediately if they develop
chest pain, increased or irregular heart rate, palpitations, nervousness, heat intolerance, diarrhea, sweating, or
irritability. Women who are pregnant, breastfeeding, or planning to get pregnant should notify their healthcare
provider.6
Back to Top
Encourage patients to wear a medical-alert bracelet or medal. Tell them not to consume large amounts of the
following foods, which can prevent thyroid hormone secretion: strawberries, peaches, pears, cabbage, spinach,
turnips, peas, cauliflower, and radishes.6
Staying in balance
Back to Top
Thyroid disorders are complex and can affect many body systems. By knowing these interrelationships and
how to recognize hyperthyroidism and hypothyroidism and their complications, you can help patients get
appropriate care and avoid life-threatening complications.
About the thyroid 1,2,4
The thyroid is an endocrine gland found in the anterior portion of the neck, just below the cricoid cartilage. Its
two lobes are positioned on opposite sides of the trachea and are joined by a narrow band of tissue (isthmus)
that passes across the trachea anteriorly, giving the gland a butterfly-like shape. The tissue is composed of two
types of cells: follicular cells, which produces thyroxine (T4) and triiodothyronine (T3), and parafollicular cells,
which produces and secretes thyrocalcitonin (also called calcitonin).
The manufacture of thyroid hormones requires dietary ingestion of protein and iodine. An iodine deficiency
leads to decreased production ofT3 and T4, which may lead to goiter.
T3 and T4 increase metabolism, which in turn increases oxygen use and heat production by the body tissues.
Most circulating T3 and T4 are bound to plasma proteins; a smaller portion flows as free hormone that can
easily enter cells and attach to a receptor site within the cell’s nucleus. When T3 or T4 binds to this recegtor, it
turns on genes important to metabolism.
T3 is a more active thyroid hormone, so following entrance into the cell, T4 is
converted into T3. Several things may impede the conversion ofT4 to T3, including
stress, starvation, beta-blockers, amiodarone, corticosteroids, iodinated contrast
media, and PTU. Conversely, cold temperatures may increase the conversion. Figure. No
caption a …
T3 and T4 are secreted through a negative feedback mechanism involving the hypothalamus, the anterior
pituitary gland, and the thyroid gland. In response to certain stimuli such as cold temperatures and stress, the
hypothalamus secretes TRH, which prompts the anterior pituitary gland to release TSH. TSH then stimulates
the thyroid gland to produce and release the thyroid hormones. If circulating levels ofT3 and T4 are low,
release ofTSH is increased. Conversely, if circulating levels of the thyroid hormones are elevated, release of
TSH is inhibited.
Back to Top
4
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Qvid: Tipping the scales: Understanding thyroid imbalances.
Calcitonin, the other hormone produced in the thyroid gland, decreases serum calcium by reducing bone
resorption (breakdown). Calcitonin also reduces the rena l tubular reabsorption of calcium and phosphate. The
level of calcium in the blood dictates calcitonin secretion. Low calcium levels will inhibit the secretion of
calcitonin, and high calcium levels will stimulate its secretion. In addition, pregnancy, a high-calcium diet, and
increased secretion of gastrin also increase calcitonin secretion.2 Calcitonin’s actions are opposite to that of
the parathyroid hormone (PTH). PTH secretion stimulates increased bone resorption, with resu ltant elevations
in serum calcium and phosphorus level. So, through coordinated management of calcitonin and PTH release
and inhibition, the endocrine system in healthy people maintains appropriate serum levels of calcium and
phosphorus.
Serious trouble
Thyrotoxic crisis, also known as thyroid storm, is a life-threatening exacerbation of hyperthyroidism that occurs
with an undiagnosed or inadequately treated hyperthyroid state.8 Most commonly associated with Graves
disease, thyrotoxic crisis is caused by a heightened response in the catechola·mine receptor sites that
intensifies the sympathetic nervous system effects on the body. Clinical manifestations of hyperthyroidism are
exaggerated in this crisis state and include fever, cardiovascular changes (chest pain, tachycardia,
hypertension, heart failure), and neurologic issues (agitation, confusion, delirium). Without prompt treatment,
patients can die from heart failure.1 ,3,4
For patients who develop thyrotoxic crisis, rapid diagnosis and treatment is key to reducing mortality. It’s also
important to identify and treat (whenever possible) the acute event that often precipitates it, such as infection.
Apply cooling blankets and ice packs to aggressively treat hyperpyrexia. Acetaminophen should be used
instead of aspirin, which can increase serum free T3 and T4 levels by interfering with their protein binding.15
Administer replacement fluids, electrolytes, and glucose as prescribed to maintain normal serum levels.
The therapeutic regimen typically consists of:
* beta-blockers to control signs and symptoms of increased adrenergic tone and reduce myocardial oxygen
demands.
*a thionamide to block thyroid hormone synthesis. PTU is the most effective drug to block thyroid synthesis
but normally is administered orally. If the patient can’t take anything orally, PTU may be administered rectally.
*an iodine solution to block thyroid hormone release.
Back to Top
* glucocorticoids or an iodinated radiocontrast agent to reduce the conversion ofT4 to T3 and promote
vasomotor stability.6, 15
REFERENCES:
1. Porth C. Matfin G. Pathophysiology: Concepts of Altered Health States. 8th ed. Philadelphia, PA: lippincott
Williams & Wilkins; 2010. [Context Link]
2. lgnatavicius D, Workman L. Medical-Surgical Nursing: Critical Thinking for Collaborative Care. 6th ed.
Philadelphia, PA: Elsevier Saunders; 2010. [Context Link]
3. Sole ML, Klein DG, Moseley MJ. Introduction to Critical Care Nursing. 5th ed. St. Louis, MO: Saunders; 2009.
[Context Link]
4. Urden LD, Stacy KM, Lough ME. Critical Care Nursing: Diagnosis and Management. 6th ed. St. Louis, MO:
Elsevier Mosby; 2010. [Context Link]
5. Hegedus L. Treatment of Grave’s hyperthyroidism: evidence-based and emerging modalities. Endocrinol
Metab Clin North Am. 2009;38(2):355-371. [Context Link]
6. Adams M, Koch R. Pharmacology: Connections to Nursing Practice. Upper Saddle River, NJ: Pearson; 2010.
[Context Link]
7. Smeltzer SC, Bare BG, Hinkle JL, Cheever KH. Textbook of Medical-Surgical Nursing. 11th ed. Philadelphia, PA:
lippincott Williams & Wilkins; 2008. [Context Link]
8. Longo D, Fauci A, Kasper D, Hauser S, jameson J, Loscalzo j. Harrison’s Principles of Internal Medicine. 18th ed.
New York, NY: McGraw-Hill Professional; 2011. [Context Link]
9. Davies TF. Pathogenesis and clinical features of Grave’s ophthalmopathy (orbitopathy). 2012. UpToDate.
http://www.uptodate.com
. [Context Link]
10. Woolever DR, Beutler AI. Hypothyroidism: a review of the evaluation and management. Fam Pract Recert.
2007;29(4):45-52. [Context Link]
11. Ross DS. Disorders that cause hypothyroidism. 2012. UpToDate.
5
http:/ /ovidsp.tx.ovid.corn. whccd.idrn.oclc.org/sp-3 .16.0b/ovidweb.cgi?&S=BPBEFPECAP… 8/25/2015
Ovid: Tipping the scales: Understanding thyroid imbalances.
http://www.uptodate.com
. [Context Link]
12. Wu P. Practical pointers: thyroid disease and diabetes. Clinical Diabetes. 2000;18(1):38.
http://journal.diabetes.org/clinicaldiabetes/v18n12000/pg38.htm
. [Context Link]
13. Hodgson B, Kizior R. Saunders Nursing Drug Handbook 2012. St. Louis, MO: Elsevier Saunders; 2012. [Context
Link]
14. Ross DS. Treatment of hypothyroidism. 2012. UpToDate.
http://www.uptodate.com
. [Context Link]
15. Ross DS. Thyroid storm. 2012. UpToDate.
http://www.uptodate.com
. [Context Link]
16. Ross DS. Myxedema coma. 2012. UpToDate.
http://www.uptodate.com
. [Context Link]
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How Hyperthyroidism and Hypothyroidism affect our Body

Order Description

SUMMARIZE THIS ARTICLE.(use attached article).
Direction to follow: Due Sept 20, 2015
New Title: How Hyperthyroidism and Hypothyroidism affect our Body
1 .Use only this Article (no outside resources to use).
2. APA format with Title on every header by page number. Need Abstract.
3. Summarize the Article (3 pages only double spaces). For Conclusion put reason why chosen this article.
4. Reference (use only the authors of this article).
5. Check for plagiarism.

How Hyperthyroidism and Hypothyroidism …
Oyid: Tipping the scales: Understanding thyroid imbalances. 1
/f.1/J1_h!h/d! ~. &111()-t~-
. Wolters Kluwer Ovid@ My Account My PayPerView Support & Training Help Logoff
Search journals Multimedia My Workspace
< Back to Search Results
Hide Cover
[Featu re]
Nursing Critical Care
Issue: Volume 8(1 ). january 2013, p 23-28
Copyright: © 2013 lippincott Will iams & Wilkins, Inc.
Publication Type: [Feature]
DOl: 10.1 097/01.CCN .0000418818.21604.22
ISSN: 1558·447X
Accession: 01244666·201301 000-00006
< Previous Article Table of Contents
Tipping the scales: Understanding thyroid imbalances
Crawford, Ann PhD, RN; Harris, Helene MSN, RN
Author Information
Next Article >
Ann Crawford is a professor in the College of Nursing at the University of Mary Hardin-Baylor in Belton, Tex.
Helene Harris is a clinical educator at Central Texas Veterans Health care System in Temple, Tex.
Find out how to recognize and respond to potentially life-threatening metabolic imbalances.
The authors have disclosed that they have no financial relationships related to this article.
Thyroid hormones affect overall metabolism and electrolyte balance. Alterations in
thyroid hormone function can cause widespread and potentially life-threatening
effects. This article reviews hyperthyroidism and hypothyroidism and what you need
to know about each condition. For details on this endocrine gland, see About the
thyroid.
~RTHYROID~
Figure. No
caption a …
Hyperthyroidism is the clinical syndrome that results when tissues are exposed to high levels of circulating
thyroid hormone. In most cases, hyperthyroidism is due to hyperactivity of the thyroid gland.1 This common
endocrine disorder can occur at any age, although patients typically are diagnosed between ages 20 and 40.
Women are much more likely to be diagnosed with a form of hyperthyroidism than men.2,3 The increased
levels of circulating thyroid hormones increase sympathetic nervous system activity and increase metabolic
rate, causing many of the clinical manifestations of hyperthyroidism.1
Thyroid hormone overstimulation on the cardiovascular system causes “fight-or-flight” types of responses,
including an increase in heart rate, stroke volume, myocardial contractility, and BP.1 ,2 No matter what the
cause, manifestations of overproduction of thyroid hormones are termed thyrotoxicosis. However,
thyrotoxicosis isn’t synonymous with hyperthyroidism and thyrotoxicosis can occur without hyperthyroidism.
For a list of the manifestations of hyperthyroidism, see Clinical manifestations of hyperthyroidism and
hypothyroidism.
Elevated thyroid hormone levels increase the body’s metabolic rate and affect the metabolism of proteins, fat s,
and carbohydrates. Because of th is, although the patient has an increased appetite and food intake, energy
needs exceed the supply and the person loses weight. With the high metabolic rate, protein degradation
exceeds protein synthesis, causing a negative nitrogen balance. Fat metabolism is increased, reducing fat
stores. Sustained hyperthyroidism leads to more chronic nutritional deficits.1 ,2 Hypersecretion of thyroid
hormones can also affect the secretion of other endocrine hormones within the hypothalamus and anterior
pituitary gland, including sex hormone production.2
Thyrotoxicosis may also be caused by radiation exposure, ingestion of excess thyroid hormone, thyroiditis
(usually temporary), interferon-alpha therapy, pituitary tumors, and metastatic thyroid cancer. Patients taking
the antiarrhythmic drug amiodarone, a heavily iodinated compound, can develop hyperthyroidism or
hypothyroidism.3 Hyperthyroidism may be acute or chronic, depending on its underlying etiology.
Graves disease is an autoimmune disease, characterized by abnormal stimulation of the thyroid gland, in which
the body makes antibodies that bind to the thyro id-stimulation hormone (TSH) receptor sites in the thyroid.
Thyroid-stimulating immunoglobulins (TS is) attach to the thyroid tissue, causing gland hypertrophy and thyroid
hormone overproduction. Patients with Graves disease will demonstrate the key features of thyrotoxicosis.1 ,3
<Previous Result Next Result >
Tools
)…. Article as PDF (226KB)
Complete Reference
e Print Preview
141 Email jumps tart
G3l Ema il PDF j umpstart
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~ Find Sim il ar
About this journal
Request Permissions
Outline
HYPERTHYROIDISM
Diagnostic testing and
management
Nursing considerations and
patient teaching
HYPOTHYROIDISM
Diagnostic testing and
management
Nursing interventions
Patient education
Staying in balance
About the thyroid ..
Serious trouble
REFERENCES:
IMAGE GALLERY
http://ovidsp.tx.ovid.corn.whccd.idm.oclc.org/sp-3.16.0b/ovidweb.cgi?&S=BPBEFPECAP … 8/25/2015 ‘
Ovid: Tipping the scales: Understanding thyroid imbalances.
Back to Top
Toxic multinodulor goiter is hyperthyroidism caused by multiple thyroid nodules. usually composed of enlarged
thyroid tissue or benign tumors. The overproduction of thyroid hormones is usually less severe than in Graves
disease, and the clinical presentation wilt be similar, though without the manifestation of exophthalmos or
pretibial edema.2
Diagnostic testing and management — Table Clinical man if…
Hyperthyroidism is diagnosed based on patient history, clinical presentation, and thyroid hormone lab studies,
and including T3, T4, TSH, and T3 resin uptake (T3RU). In addition, measurement ofTSH receptor antibodies
(TSH-RAb) may be used to diagnose Graves disease.2
A radioiodine uptake and thyroid scan may be performed to evaluate the thyroid gland’s size, position, and
function. A thyroid ultrasound may also be used to determine the size of the thyroid gland and presence of
masses or nodules.2,4
Treatment for hyperthyroidism includes antithyroid drug therapy, radioiodine, and surgery (subtotal or neartotal
thyroidectomy).S Medications such as methimazole and propylthiouracil (PTU) inhibit the synthesis of
thyroid hormones, but don’t inactivate circulating thyroid hormones or those stored in the thyroid. These
medications are used for long-term management. Potassium iodide and iodine solutions inhibit the synthesis
and the release of the thyroid hormone, and generally are used for short-term therapy, such as before thyroid
surgery.6 Beta-blockers can be used to help control adrenergic signs and symptoms, especially in the early
stages of treatment before the antithyroid drugs take effect. Beta-blockers block the effects of the thyroid
hormone on the sympathetic receptors of the heart, decreasing myocardial oxygen demands.6
Radioiodine (radioactive iodine) causes progressive destruction of thyroid cells . Potential adverse effects
include pharyngitis or neck tenderness for a few days, and complications include hypothyroidism.6 Radioiodine
may exacerbate the ophthalmopathy for patients with Graves disease (more on this later).6 Because fewer
than 50% of patients treated with antithyroid medications remain in long-term remission, radioactive iodine is
used increasingly as a permanent treatmentS
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Surgery, once a primary method of treating hyperthyroidism, is reserved today for patients with special
circumstances, such as inability to take antithyroid medication, pregnancy, a large goiter, or
ophthalmopathy.2,5 Most of the thyroid gland is removed, permanently reducing thyroid hormone production.
Following the surgery, patients usually must take thyroid replacement medication daily to prevent
hypothyroidism.5,7 Major complications of surgery include bleeding, laryngeal edema, hypoparathyroidism,
and recurrent laryngeal nerve damage.8
Nursing considerations and patient teaching
Monitor the patient’s vital signs closely; an alteration in metabolic rate can lead to significant increases in heart
rate, BP, and temperature. Assess all body systems and monitor food intake, appetite, and weight. Assess
muscle strength and watch for tremors, heat intolerance, emotional changes, and irritability, which could
indicate thyrotoxicosis. Assess and document intake and output.
Monitor the patient’s thyroid hormone levels (to determine if antithyroid medications are effective, and to
monitor for increasing symptomology), as welt as liver function tests. Some antithyroid drugs can cause
leukopenia, agranulocytosis, and other hematologic dysfunction, so monitor the patient’s complete blood celt
count and lactate dehydrogenase. Closely monitor serum glucose and electrolyte levels, especially in patients
exhibiting manifestations of thyrotoxic crisis (for more on thyrotoxic crisis, see Serious trouble).6
Iodine toxicity can occur if the patient is taking too much iodine or the dose is too high. Signs of iodine toxicity
include burning sensation in the mouth and throat, metallic taste in the mouth, sore teeth and gums, increased
salivation, nasal discharge, gastrointestinal upset, and periorbital edema. Teach patients to report these
symptoms to their hea lthca re provider immediately. Because antithyroid medications work to decrease thyroid
function, be alert for manifestations of hypothyroidism.6 Consult the full prescribing information for details
about drugs your patient is prescribed.
Encourage patients to have regular follow-up appointments, which wilt include monitoring their thyroid
hormone levels. Teach them to avoid foods high in iodine, such as seafood, tofu, soy, cheddar cheese,
mayonnaise, and iodized salt, and to wear a medical-alert bracelet or medal.
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Patients with Graves disease are at risk for Graves ophthalmopathy, an autoimmune disease in which
inflammation increases the volume of the extraocular muscles and retro-orbital tissues. Te ll patients to notify
their healthcare provider if they develop eye swelling or irritation, blurred vision. and excessive tearing
worsened by exposure to cold, wind, or bright lights.9
2
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~ A deficiency of thyroid hormones, hypothyroidism causes a decreased metabolic ra te. Primary hypothyroidism
(99% of diagnosed cases) is caused by autoimmune, disease, or iatrogenic destruction of the thyroid gland.
~ Iatrogenic causes include surgical removal or irradiation of thyroid tissue, or medications that suppress thyroid
function, such as antithyroid drugs and lithium. Other causes include postpartum thyroiditis, subacute
granulomatous thyroiditis, and inadequate ingestion of necessary ingredients for thyroid hormone formation
(such as iodine or tyrosine).2, 10 Amiodarone, as mentioned earlier, can cause hyperthyroidism or
hypothyroidism.3
Congenital hypothyroidism occurs in about 1 of every 5,000 births, and is a preventable cause of mental
retardation. With proper neonatal screening and treatment, this problem is easily reso lved.1 In adults with
adequate iodine intake, the most common cause of hypothyroidism is chronic autoimmune thyroiditis, or
Hashimoto disease.7, 10
Less commonly, hypothyroidism is caused by decreased secretion of thyrotropin-releasing hormone (TRH)
from the hypothalamus or decreased secretion ofTSH from the anterior pituitary gland.11 Insufficient
stimulation of the thyroid gland by TSH (central hypothyroidism) is caused by either pituitary disease
(secondary hypothyroidism) or hypothalamic disease (tertiary hypothyroidism).11
Hypothyroidism occurs most often in women, and is usually diagnosed between the ages of 30 and 60 .2,7
Overall, hypothyroidism is more common than hyperthyroidism.12
In hypothyroidism, low circulating levels of thyroid hormone cause a generalized slowing of metabolic
processes. Low thyroid hormone levels stimulate the anterior pituitary gland to release TSH in an attempt to
trigger the production of more thyroid hormones. TSH binds to the thyroid tissue and over time causes goiter,
an abnormal enlargement of the thyroid gland, although it doesn’t necessarily promote increased thyroid
hormone production.1 ,2, 10 The low metabolic rate has an effect on most tissues and organs. As cellular energy
diminishes, metabolites (called glycosaminoglycans) build up within the cells, forming a cellular edema of water
mixed with mucus, known as myxedema. This non-pitting edema develops throughout the body, most
conspicuously around the eyes, in the hands and feet, and between the scapulae. The tongue appears
enlarged and the patient’s voice may sound husky or hoarse due to laryngeal edema.2
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Clinical manifestations of hypothyroidism are caused by the decreased metabolic rate. Because
hypothyroidism often occurs slowly, the onset of signs and symptoms is insidious and develops over months to
years.2 Because many of the clinical manifestations are vague, nonspecific, and slow to develop, they may be
ignored or unnoticed by patients and their families .1,2,10
Diagnostic testing and management
As with hyperthyroidism, diagnosis for hypothyroidism is based on patient history, clinical manifestations, and
serum thyroid hormone levels and TSH. In overt primary hypothyroidism, serum TSH is elevated and T3 and T4
levels are decreased. In subclinical primary hypothyroidism, serum TSH levels are high and T3 and T4 levels are
normal.4, 10,11
The treatment of choice for hypothyroidism is thyroid hormone replacement with levothyroxine, a synthetic
form ofT4. Levothyroxi ne has the same effects as the body’s own thyroid hormone, increasing the metabolic
rate, which in turn increases the heart rate; respiratory rate; BP; and fat, protein, and carbohydrate
metabolism.6 Adverse reactions to levothyroxine are potentially serious and may mimic the manifestations of
hyperthyroidism.6
Use levothyroxine cautiously in older adults, and patients with cardiovascular disease, hypertension, or
diabetes. Patients with aspirin allergy, adrenal insufficiency, and severe cardiovascular disease shouldn’t take
levothyroxine .13
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Other medications for treating hypothyroidism include desiccated thyroid extract (pork or beef), liothyronine
(T3), and liotrix (4:1 mixture ofT4 and T3).14
Nursing interventions
Obtain a health history and perform medication reconci liation, including all prescription and over-the-counter
medications, as well as herbal and nutritional supplements. Monitor vital signs regularly, and thoroughly
assess the patient’s physiologic status, including cardiovascular status, neurologic status, pulmonary status,
and renal function. To help determine nutritional status, ask patients what they’ve weighed in the past. Weigh
the patient; monitor appetite and food intake levels, as well as overall intake and output. Monitor serum
thyroid hormone levels, blood urea nitrogen and creatinine, and blood glucose, as well as prothrombin time
and international normalized ratio if the patient is on anticoagulants (levothyroxine can affect blood glucose
levels in patients with diabetes and can alter the effects of anticoagulants).
3
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Ovid: Tipping the scales: Understanding thyroid imbalances.
Monitor for continued signs of hypothyroidism that may indicate a need to increase the medication dosage,
and signs of hyperthyroidism that may indicate a need to decrease the dosage. Use appropriate patient safety
measures, and assist with ambulation and activities of daily living as needed.6
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Myxedema coma is a rare, life-threatening emergency that occurs due to unrecognized, untreated, or
undertreated hypothyroidism, and is often seen in older adults (usually women) in the winter months. The
patient will exhibit a worsening of hypothyroidism signs and symptoms (hypothermia, bradycardia,
hypotension, hypoventilation, hyponatremia, hypoglycemia, and metabolic acidosis), deteriorating
neurologically to a comatose state.16 Diminished metabolism causes respiratory depression, cardiovascular
collapse, and shock. 2,4,7 Treatment of myxedema coma includes mechanical ventilation, thyroid replacement
therapy, fluid and vasopressor administration, passive rewarming, and I.V. dextrose. However, even with
aggressive treatment, mortality is high.2,4,7
Patient education
Teach patients that thyroid replacement therapy must be taken for life, and not to discontinue medication or
change brands or dosages without contacting their healthcare provider. Because thyroid medications can
cause insomnia if taken at night, they’re usually administered in the morning on an empty stomach. Because
iron and calcium supplements and antacids can decrease absorption of levothyroxine, patients shouldn’t take
these supplements or antacids within 4 hours of taking levothyroxine. Patients should follow up with their
healthcare provider regularly, including assessment of serum thyroid hormone levels.
Teach patients to change positions slowly and to notify their healthcare provider immediately if they develop
chest pain, increased or irregular heart rate, palpitations, nervousness, heat intolerance, diarrhea, sweating, or
irritability. Women who are pregnant, breastfeeding, or planning to get pregnant should notify their healthcare
provider.6
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Encourage patients to wear a medical-alert bracelet or medal. Tell them not to consume large amounts of the
following foods, which can prevent thyroid hormone secretion: strawberries, peaches, pears, cabbage, spinach,
turnips, peas, cauliflower, and radishes.6
Staying in balance
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Thyroid disorders are complex and can affect many body systems. By knowing these interrelationships and
how to recognize hyperthyroidism and hypothyroidism and their complications, you can help patients get
appropriate care and avoid life-threatening complications.
About the thyroid 1,2,4
The thyroid is an endocrine gland found in the anterior portion of the neck, just below the cricoid cartilage. Its
two lobes are positioned on opposite sides of the trachea and are joined by a narrow band of tissue (isthmus)
that passes across the trachea anteriorly, giving the gland a butterfly-like shape. The tissue is composed of two
types of cells: follicular cells, which produces thyroxine (T4) and triiodothyronine (T3), and parafollicular cells,
which produces and secretes thyrocalcitonin (also called calcitonin).
The manufacture of thyroid hormones requires dietary ingestion of protein and iodine. An iodine deficiency
leads to decreased production ofT3 and T4, which may lead to goiter.
T3 and T4 increase metabolism, which in turn increases oxygen use and heat production by the body tissues.
Most circulating T3 and T4 are bound to plasma proteins; a smaller portion flows as free hormone that can
easily enter cells and attach to a receptor site within the cell’s nucleus. When T3 or T4 binds to this recegtor, it
turns on genes important to metabolism.
T3 is a more active thyroid hormone, so following entrance into the cell, T4 is
converted into T3. Several things may impede the conversion ofT4 to T3, including
stress, starvation, beta-blockers, amiodarone, corticosteroids, iodinated contrast
media, and PTU. Conversely, cold temperatures may increase the conversion. Figure. No
caption a …
T3 and T4 are secreted through a negative feedback mechanism involving the hypothalamus, the anterior
pituitary gland, and the thyroid gland. In response to certain stimuli such as cold temperatures and stress, the
hypothalamus secretes TRH, which prompts the anterior pituitary gland to release TSH. TSH then stimulates
the thyroid gland to produce and release the thyroid hormones. If circulating levels ofT3 and T4 are low,
release ofTSH is increased. Conversely, if circulating levels of the thyroid hormones are elevated, release of
TSH is inhibited.
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Qvid: Tipping the scales: Understanding thyroid imbalances.
Calcitonin, the other hormone produced in the thyroid gland, decreases serum calcium by reducing bone
resorption (breakdown). Calcitonin also reduces the rena l tubular reabsorption of calcium and phosphate. The
level of calcium in the blood dictates calcitonin secretion. Low calcium levels will inhibit the secretion of
calcitonin, and high calcium levels will stimulate its secretion. In addition, pregnancy, a high-calcium diet, and
increased secretion of gastrin also increase calcitonin secretion.2 Calcitonin’s actions are opposite to that of
the parathyroid hormone (PTH). PTH secretion stimulates increased bone resorption, with resu ltant elevations
in serum calcium and phosphorus level. So, through coordinated management of calcitonin and PTH release
and inhibition, the endocrine system in healthy people maintains appropriate serum levels of calcium and
phosphorus.
Serious trouble
Thyrotoxic crisis, also known as thyroid storm, is a life-threatening exacerbation of hyperthyroidism that occurs
with an undiagnosed or inadequately treated hyperthyroid state.8 Most commonly associated with Graves
disease, thyrotoxic crisis is caused by a heightened response in the catechola·mine receptor sites that
intensifies the sympathetic nervous system effects on the body. Clinical manifestations of hyperthyroidism are
exaggerated in this crisis state and include fever, cardiovascular changes (chest pain, tachycardia,
hypertension, heart failure), and neurologic issues (agitation, confusion, delirium). Without prompt treatment,
patients can die from heart failure.1 ,3,4
For patients who develop thyrotoxic crisis, rapid diagnosis and treatment is key to reducing mortality. It’s also
important to identify and treat (whenever possible) the acute event that often precipitates it, such as infection.
Apply cooling blankets and ice packs to aggressively treat hyperpyrexia. Acetaminophen should be used
instead of aspirin, which can increase serum free T3 and T4 levels by interfering with their protein binding.15
Administer replacement fluids, electrolytes, and glucose as prescribed to maintain normal serum levels.
The therapeutic regimen typically consists of:
* beta-blockers to control signs and symptoms of increased adrenergic tone and reduce myocardial oxygen
demands.
*a thionamide to block thyroid hormone synthesis. PTU is the most effective drug to block thyroid synthesis
but normally is administered orally. If the patient can’t take anything orally, PTU may be administered rectally.
*an iodine solution to block thyroid hormone release.
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* glucocorticoids or an iodinated radiocontrast agent to reduce the conversion ofT4 to T3 and promote
vasomotor stability.6, 15
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Philadelphia, PA: Elsevier Saunders; 2010. [Context Link]
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9. Davies TF. Pathogenesis and clinical features of Grave’s ophthalmopathy (orbitopathy). 2012. UpToDate.
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11. Ross DS. Disorders that cause hypothyroidism. 2012. UpToDate.
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16. Ross DS. Myxedema coma. 2012. UpToDate.
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. [Context Link]
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