Thyroid Dysfunction Nursing CE Course

2.0 ANCC Contact Hours AACN Category A

Syllabus

Objectives

By the completion of this exercise, the learner will be able to:

  1. Understand normal function of the thyroid gland and differentiate the types of thyroid dysfunction.
  2. Discuss the epidemiology and etiology of thyroid dysfunction.
  3. Explain the pathophysiology and clinical manifestations of thyroid dysfunction.
  4. Understand the diagnostic studies for thyroid dysfunction.
  5. Explain collaborative care and nursing management of the patient with thyroid dysfunction.
  6. Identify complications related to thyroid dysfunction.

Introduction

The thyroid gland is located in the anterior neck. As seen in Figure 1, it lies in front of the trachea, just below the larynx and is shaped like a butterfly. The gland weighs approximately 20-60 grams. The gland is composed of several lobules that contain follicles, which are small, secretory glands. These follicles store thyroid hormones in the form of droplets (How Does the Thyroid Gland Work, 2018).

The thyroid gland plays a vital role in maintaining equilibrium in the body. Hormones secreted by the thyroid affect metabolism, growth, and development. Specifically, metabolic rate, oxygen consumption, body temperature, caloric needs, carbohydrate and fat metabolism, and brain and nervous system function are affected by thyroid hormones (Kelly, 2017). The thyroid gland produces three different hormones (see Figure 2 below). Two hormones produced and secreted by the thyroid gland are triiodothyronine (T3) and tetraiodothyronine or thyroxine (T4). The follicular epithelial cells of the thyroid produce T3 and T4 (2018). T4 makes up 90% of the thyroid hormone produced by the thyroid gland; however, T3 has a much higher potency and more significant metabolic effect (Kelly, 2017). A large portion of the T4 released into the bloodstream converts into T3. Approximately 80% of T3 is from this conversion, while the thyroid gland secretes the remaining 20% of T3 directly (Kelly, 2017). Iodine is an essential need for this hormone production. Our body does not produce endogenous iodine, so it is vital to get iodine from our diet. Dietary iodine is absorbed through the bowel, then directed to the thyroid gland to be utilized in hormone production (Taylor et al., 2018). Calcitonin is the third hormone produced by the thyroid gland. However, it differs from T3 and T4 as it is produced by parafollicular cells (C cells) of the thyroid gland. Calcitonin plays a role in calcium regulation. Calcitonin reacts to decrease hypercalcemia levels in the blood (Kelly, 2017).

The pituitary gland has a direct relationship with the thyroid gland. Thyroid stimulating hormone (TSH) is produced and secreted by the anterior pituitary gland. The hypothalamus is alerted when there are low circulating levels of T3, T4, and calcitonin. In response, the hypothalamus releases thyrotropin-releasing hormone (TRH). This hormone causes the pituitary gland to release TSH. The opposite effect occurs when there are high circulating thyroid hormones, and TRH and TSH are both inhibited (Kelly, 2017). 

The two most common disorders of the thyroid gland are hypothyroidism and hyperthyroidism. Hypothyroidism is a scarcity of the thyroid hormone that causes a general slowing of the metabolic rate. Hyperthyroidism is an overactive state of the thyroid gland with a constant increase in the production and release of thyroid hormones (Kelly, 2017).


Etiology and Epidemiology

Worldwide, the most common cause of hypothyroidism is iodine deficiency. In the United States, there are several options for iodine intake. Common ways Americans ingest iodine are through iodized table salt, shellfish, eggs, soymilk, cow’s milk, and cheese (American Thyroid Association, n.d.). 


The most common type of hypothyroidism in the United States is primary hypothyroidism caused by atrophy of the thyroid gland, often secondary to an autoimmune disease (Kelly, 2017). Patients with autoimmune diseases such as type 1 diabetes and celiac disease are more likely to develop hypothyroidism.


The vast majority of hyperthyroidism cases (75%) are related to Graves’ disease. Graves’ disease is an autoimmune disease of unknown etiology. Women are five times more prone to developing Graves’ disease than men. Hyperthyroidism occurs most frequently between the ages of 20 to 40 (Kelly, 2017).


As estimated by the American Thyroid Association (n.d.), 20 million Americans have a type of thyroid dysfunction, and 60% of these individuals are unaware of their condition. One in eight women will develop a thyroid problem during her lifetime. Women have a five to eight times higher likelihood than men of developing thyroid problems. Though thyroid dysfunction is a somewhat common problem, it can be diagnosed and treated quickly. However, left undiagnosed, it can have detrimental side effects and may lead to death (Taylor et al., 2018).

Pathophysiology and Risk Factors

Hypothyroidism, often referred to as thyroid hormone deficiency, is the most common type of thyroid dysfunction. Hypothyroidism is classified as primary or secondary. Primary hypothyroidism is caused by the destruction of the thyroid gland or tissue. Primary can also be due to defective hormone synthesis. Most often, the TSH level is elevated due to the pituitary gland trying to signal the thyroid gland to make more thyroid hormones (Kelly, 2017). 

Pituitary gland dysfunction or hypothalamic disease is the cause of secondary hypothyroidism. This dysfunction causes a decreased secretion of TSH and TRH, which then leads to reduced T3 or T4 serum levels.

As previously mentioned, worldwide, iodine deficiency is a leading cause of primary hypothyroidism. In the United States, Hashimoto's disease is the most common cause of hypothyroidism. Hashimoto's is chronic, autoimmune thyroiditis (Chaker, Bianco, Jonklas, & Peeters, 2017). When a patient has Hashimoto’s thyroiditis, their immune cells gradually attack the thyroid. The process is gradual, so some patients may never be symptomatic. As Hashimoto’s becomes more advanced, the patient develops a significantly elevated TSH, with a marked decrease in T3 and T4 (Ledesma & Lawson, 2018). 

Hypothyroidism can also develop due to the destruction of the thyroid gland from certain drugs. Amiodarone (Cordarone, a class III antiarrhythmic medication) has a very high iodine content and can destroy the thyroid gland by blocking T3, T4, and calcitonin production (Ross, 2018). Approximately 14% of patients taking amiodarone (Cordarone) develop hypothyroidism (Chaker et al., 2017). 

The drug lithium (Lithobid, an antipsychotic medication) may cause hypothyroidism. Lithium (Lithobid) blocks thyroid hormone synthesis, and approximately 50% of patients taking it develop a goiter (enlarged thyroid gland). Goiter formation usually occurs within the first two years of lithium (Lithobid) treatment (Surks, 2019). 

Cretinism is hypothyroidism that develops during infancy due to a lack of thyroid hormone during fetal or neonatal life. In the United States, all infants are screened for thyroid dysfunction at birth (Kelly, 2017).

Patients with hypothyroidism or hyperthyroidism can have lymphocytes that produce antibodies that fight against their thyroid. These antibodies can either damage or destroy the gland or stimulate activity. The two most common antibodies that cause thyroid dysfunction are thyroid peroxidase and thyroglobulin. “Positive antithyroid peroxidase or anti-thyroglobulin antibodies in a patient with hypothyroidism make a diagnosis of Hashimoto's thyroiditis. If the antibodies are positive in a hyperthyroid patient, the most likely diagnosis is autoimmune thyroid disease," such as Graves' disease (American Thyroid Association, n.d.).

Hyperthyroidism is a hyperactive clinical syndrome of the thyroid gland characterized by an increased free serum T3 or T4. Thyrotoxicosis is defined as excess thyroid hormones in the body. With increased T3 or T4, the TSH is low because the pituitary gland senses there are adequate amounts of thyroid hormone in the body. Hyperthyroidism can develop due to thyroiditis, excessive iodine intake, pituitary tumors, thyroid cancer, and toxic nodular goiters (enlarged gland with varying nodule sizes that show hyperplasia). However, the most common form is Graves’ disease (Kelly, 2017).

Graves’ disease is an autoimmune disease with a distinct thyroid relationship. The immune system reacts inaccurately by producing antibodies that overstimulate the thyroid gland. Patients with a diagnosis of Graves’ disease have diffuse thyroid enlargement and a marked increase in T3 or T4 (Kelly, 2017).

A patient can develop a goiter with either hypothyroidism or hyperthyroidism. As previously mentioned, a goiter is an enlarged thyroid gland. If a patient develops a goiter, lab tests are performed to determine the type and cause. Goitrogens are foods or medications that may cause a goiter to develop. See the list below of goitrogens.

Medications:

  • Propylthiouracil (PTU)
  • Methimazole (Tapazole)
  • Large doses of iodine
  • Sulfonamides
  • Salicylates
  • P-Aminosalicylic acid
  • Lithium (Lithobid)
  • Amiodarone (Cordarone)

Foods:

  • Broccoli
  • Brussels sprouts
  • Cabbage
  • Cauliflower
  • Kale
  • Mustard
  • Peanuts
  • Strawberries
  • Turnips (Kelly, 2017).

Clinical Manifestations

Hypothyroidism

Thyroid dysfunction often comes with many life-altering symptoms. In hypothyroidism, the clinical manifestations are a result of the slowing body processes (see Figure 2 below). Manifestations diverge depending on the severity and extent of thyroid deficiency, as well as the patient's age at the time the deficiency is diagnosed. Symptoms may develop gradually over months to years unless hypothyroidism occurs after a thyroidectomy, thyroid ablation, or as a result of hyperthyroidism medications (antithyroid drugs). The most common symptoms of hypothyroidism are weight gain, cold intolerance, lethargy, fatigue, dry and flaky skin, hoarseness, and constipation (Chaker et al., 2017).  Many patients diagnosed with hypothyroidism have cognitive, and personality changes and may appear depressed. With the mental changes, patients may experience memory loss, decreased motivation, and slowed speech. In the geriatric patient, many of these symptoms are attributed to aging. If there is a new onset of these symptoms in the geriatric patient, the patient should be evaluated for thyroid dysfunction. Less common neurocognitive changes include neuropathy, decreased smell sensation, and hearing impairment (Kelly, 2017).

In addition to the most common manifestations, patients with a diagnosis of hypothyroidism may also have specific organ-related manifestations. Cardiovascular symptoms may include shortness of breath or dyspnea on exertion. Patients may also develop hyperlipidemia, hypertension, bradycardia, decreased cardiac output, and arrhythmias. Patients with a pre-existing cardiac disease are at higher risk for these complications. Kidney function may also be affected by a reduced glomerular filtration rate (Chaker et al., 2017).

Patients with chronic, severe hypothyroidism may develop myxedema. Myxedema is the changing physical appearance of the skin and subcutaneous tissues (see Figure 3 below) due to the accumulation of hydrophilic mucopolysaccharides in the dermis and surrounding tissues. This edema causes periorbital (around the eyes) edema, facial puffiness, and a masklike face. Many individuals with myxedema struggle with an altered self-image (Kelly, 2017).

Hyperthyroidism

In contrast to hypothyroidism, hyperthyroidism is characterized by a hyperactive thyroid hormone synthesis and secretion. Common complaints among patients diagnosed with hyperthyroidism are tremors, anxiety, palpitations, fatigue (often due to insomnia), weight loss, polydipsia (increased urination), diaphoresis (excessive sweating), and heat intolerance (De Leo, Lee, & Braverman, 2016).

As previously stated, Graves’ disease accounts for the majority of cases of hyperthyroidism. Approximately 25% of patients diagnosed with Graves’ disease develop exophthalmos (bilateral protrusion of eyeballs). A goiter (enlarged thyroid gland) may also be palpable or evident upon inspection (De Leo et al., 2016) See Figure 4 below, demonstrating exophthalmos and goiter.

Acropachy is another type of extrathyroidal manifestation. It is rarer than exophthalmos. If a patient develops acropachy, they exhibit digital clubbing and edema of the fingers (Kelly, 2017). In addition to these clinical manifestations, see Table 1 below for other parts of the body that may be affected by thyroid dysfunction.

Table 1: Manifestations of Thyroid Dysfunction


Diagnostics

Any patient with suspected thyroid dysfunction should have a detailed history and physical performed. The nurse should focus the assessment on any reported symptoms that are characteristic of thyroid disease. When assessing for thyroid dysfunction, the most reliable laboratory tests are TSH, free T4, and T3. Normal reference ranges for thyroid function lab results include: 

  • TSH: 0.4-4.2 mU/L
  • T4 (total): 4.5-11 µg/dL 
  • T4 (free): 0.8-2.7 ng/dL
  • T3 in adults < 50: 70-204 ng/dL 
  • T3 in adults> 50: 40-181 ng/dL (Kelly, 2017).

Serum TSH is the most common initial screening test to evaluate the thyroid. Combining the serum TSH and free T4 results (see Table 2 below) more accurately determines how the thyroid gland is functioning (American Thyroid Association, n.d.). A diagnosis of primary hypothyroidism would typically include an increased TSH, a decreased free T4, and possibly a reduced T3. Secondary hypothyroidism will most likely present with a decreased TSH and T4. Other laboratory findings that are common with a diagnosis of hypothyroidism are elevated triglycerides and cholesterol, increased creatine kinase, and anemia (decreased hemoglobin/hematocrit) (Kelly, 2017).

Lab testing results in a patient with hyperthyroidism often consist of an extremely low or undetectable TSH and increased T3 or T4 (Kelly, 2017). The nurse should keep in mind that these are the expected values in patients that are undiagnosed or untreated. 

Table 2: Interpretation of Thyroid Function Tests


Hyperthyroidism

Primary Hypothyroidism

Secondary Hypothyroidism

TSH

Decreased (<0.4)

Elevated (>4.2)

Decreased (<0.4)

Free T4

Elevated (>2.7)

Decreased (<0.8)

Decreased (<0.8)

(American Thyroid Association, n.d.)

A radioactive iodine uptake (RAIU) test can diagnose hyperthyroidism or hypothyroidism. However, it is most commonly used to differentiate Graves’ disease from other forms of hyperthyroidism (Kelly, 2017). If a patient is taking levothyroxine (Synthroid), it should be discontinued four weeks before an RAIU test (Skidmore-Roth, 2015). This diagnostic test requires the patient to swallow a small amount of radioactive iodine. The test measures the amount of radioactivity that is taken up by the thyroid gland, which determines thyroid function (American Thyroid Association, n.d.). The patient with a diagnosis of Graves’ disease shows a diffuse uptake of 35% to 95%. A normal result would show a radioactive uptake of 25% or less. (Kelly, 2017).

If a patient develops a thyroid nodule or goiter, it is common for a thyroid ultrasound to be performed. The ultrasound is beneficial to determine if a nodule is cystic (fluid-filled) or solid and the exact size of the nodule. If a nodule is a concern of possible thyroid cancer, an ultrasound-guided fine needle biopsy may be performed (American Thyroid Association, n.d.).

Complications

Complications may occur with hypothyroidism or hyperthyroidism. A patient with hypothyroidism can develop myxedema coma. Myxedema coma was first described in the late 1900s as a result of long-standing, non-treated hypothyroidism. It has become a rare complication but is a medical emergency with a mortality rate of 40% (Chaker et al., 2017). Now, myxedema can occur from undiagnosed cases of hypothyroidism. It may also be precipitated by infection, certain types of drugs (most common are opioids, barbiturates, and tranquilizers), extreme cold exposure, or trauma (Kelly, 2017). Patients who develop myxedema coma will typically have altered cognition, progressive lethargy, bradycardia, and hypothermia. These manifestations can progress to multisystem organ failure and death if immediate treatment with intravenous thyroid hormone therapy is not initiated (Chaker et al., 2017).

Thyroid storm (also called acute thyrotoxicosis or thyrotoxic crisis) is an acute, rare complication of hyperthyroidism that occurs when excessive amounts of T3, T4, and calcitonin are pushed into circulation. Like myxedema coma, thyroid storm can result from trauma or stressors. Patients with hyperthyroidism are at risk when they undergo a thyroidectomy due to the manipulation of the thyroid gland (Kelly, 2017). Patients who develop thyroid storm have heightened symptoms of hyperthyroidism such as heart failure, extreme tachycardia, vomiting, diarrhea, severe hyperthermia, shock, neurocognitive changes, coma, and possibly death. The nurse should be familiar with the signs and symptoms of myxedema and thyroid storm, as early initiation of treatment is crucial to avoid fatality (Kelly, 2017).  

Treatment, Management, and Nursing Implications

Treatment of Hypothyroidism

The goal of treatment is to return the patient to a euthyroid state. Levothyroxine (Synthroid) as monotherapy is the treatment of choice (Chaker et al., 2017). Levothyroxine (Synthroid) may be given orally or intravenously, although oral therapy is preferred for maintenance treatment. For an adult under the age of 50, the average dose is 100-200mcg/day with a max dose of 200mcg/day. For an adult over the age of 50, the most common dose is 25-50mcg/day. Initial dosing in adults and treatment for pediatric patients are often weight-based. If the patient has diagnosed heart disease, levothyroxine (Synthroid) is administered at a smaller dose (Skidmore-Roth, 2015). Dosing is often increased in an asymptomatic patient at four- to six-week intervals as needed based on TSH levels. It usually takes at least eight weeks for optimal results of hormone replacement (Kelly, 2017).

Intravenous levothyroxine (Synthroid) is administered in patients who present with acute myxedema to avoid coma. The initial recommended IV dose is 200-500 mcg with recommended increases after the first 24 hours. Levothyroxine (Synthroid) must be diluted with 0.9% sodium chloride (NaCl) to a 100mcg/mL concentration. The medication should be mixed well and given through a three-way stop cock at a maximum rate of 100mcg/minute. Levothyroxine (Synthroid) is incompatible with the majority of medications and should not be added to another intravenous infusion (Skidmore-Roth, 2015). 

Before administering oral or intravenous levothyroxine (Synthroid), a detailed assessment is required. The nurse should note any changes in vital signs, chest pain, tachycardia, neurological hyperexcitability, and current thyroid laboratory values. If the patient is taking an anticoagulant, their prothrombin time (PT) should also be monitored as levothyroxine (Synthroid) can interact and cause excessive bleeding (Skidmore-Roth, 2015).

    

The nurse should educate patients taking levothyroxine (Synthroid) that the medication is not a cure, but a lifelong treatment requirement. Levothyroxine (Synthroid) is absorbed in the small intestine and should be administered in the morning before breakfast or on an empty stomach. The medication is usually a single, daily dose. If a patient is taking antacids, iron, or calcium supplements, they should be separated by at least four hours from their levothyroxine (Synthroid) administration. A patient should report any neurologic excitability symptoms or cardiac symptoms (including palpitations) to their health care provider immediately (Skidmore-Roth, 2015).

Patients undergoing treatment for hypothyroidism must understand the need for lifelong thyroid hormone replacement and regular, follow-up care. Patients should be educated to avoid cold temperatures. Skin breakdown can occur with hypothyroidism, and proper skin care and hygiene are essential to preventing lesions. Patients may complain of constipation and should be encouraged to increase activity gradually, increase fiber in their diet, use stool softeners, and develop regular bowel patterns (Kelly, 2017).

Treatment of Hyperthyroidism

Treatment options for hyperthyroidism are more complex than the recommended monotherapy for hypothyroidism. Options for treatment for hyperthyroidism include radioactive iodine therapy, drug therapy, and surgical intervention.

Radioactive iodine (RAI) therapy is the treatment of choice for non-pregnant adults with hyperthyroidism. RAI therapy is usually performed in an outpatient setting. A study by Wong, Shulkin, Gross, and Avram (2018) found of 316 hyperthyroid patients with Graves' disease; successful therapy was achieved in greater than 90% of patients through a single, calculated RAI dose. Patients receiving RAI may develop thyroiditis or parotiditis (inflammation of the parotid salivary gland). Symptoms with these complications include hoarseness, dry mouth, and throat irritation. The nurse should instruct the patient to gargle with salt water and take frequent sips of ice or water for relief (Kelly, 2017).

Patient education should also include the treatment time frame. It could take up to three months before the maximum desired effect occurs. Patients may need to take oral medications while waiting for the desired outcome from RAI. According to Kelly (2017), 80% of patients develop post-treatment hypothyroidism and require lifelong thyroid hormone replacement therapy. Patients should be aware of hypothyroidism symptoms and when to report these to their medical providers. The nurse should also review with patients how to prevent radiation exposure to others. Home precautions include:

  • Use a private toilet.
  • Flush two or three times after each use.
  • Separate laundry for washing.
  • Do not handle food for long periods while cooking for others.
  • Avoid contact with pregnant females and children for seven days post-treatment (Kelly, 2017).

The first-line drug treatment is medication in the antithyroid class. Propylthiouracil (PTU) and methimazole (Tapazole) are the first-line medications. These medications reach the thyroid gland via active transport, where they limit the synthesis of T3 and T4 (De Leo et al., 2016). Indications for antithyroid drugs are Graves’ disease (in young patients), pregnant patients with a diagnosis of hyperthyroidism, and patients needing to establish a euthyroid state before radiation or surgical intervention. Propylthiouracil (PTU) is the treatment of choice for thyrotoxicosis. It inhibits the peripheral conversion of T3 and T4 and achieves a euthyroid state more quickly than other drugs. A downside of this medication is that it must be taken three times a day. Methimazole (Tapazole) is given once a day. Patients usually see an improvement within one to two weeks of initiating drug therapy, but optimal results are seen within four to six weeks. Of all the patients taking these medications, 20-40% will experience spontaneous remediation after 6-15 months of treatment. However, patients should be warned that abruptly discontinuing the medication can cause a regression of their hyperthyroidism (Kelly, 2017). 

Iodine may be used in conjunction with other antithyroid drugs to achieve a euthyroid state. It acts by blocking the release of T3 and T4 into the bloodstream. Iodine is given short-term before surgery. It usually produces a maximum effect within one to two weeks (Kelly, 2017). In addition to achieving a euthyroid state, iodine causes less vascularity to the thyroid gland. Surgery is safer with preoperative iodine therapy. Iodine is given in a liquid form, mixed with juice or water, and sipped through a straw. Patients can develop iodine toxicity if not properly dosed. Signs of toxicity include buccal mucosa edema, excessive salivation, skin reactions, and nausea and vomiting. The prescribing provider should be notified immediately should these symptoms occur (Kelly, 2017).

If a patient experiences thyrotoxicosis and needs symptomatic relief, a beta-blocker may be prescribed. Propranolol (Inderal) or atenolol (Tenormin) are the two most common beta-blockers prescribed. These medications decrease tachycardia, nervousness, and irritability by blocking the effects of the sympathetic nervous system (Kelly, 2017).

Surgical intervention is another option for the treatment of hyperthyroidism. A thyroidectomy may be indicated for those with tracheal compression from a goiter, inadequate response to antithyroid medication therapy, or thyroid cancer (Kelly, 2017). The preferred surgical intervention is a subtotal thyroidectomy (see Figure 5 below).

Generally, the goal of surgery is to remove 90% of the thyroid. If a subtotal or partial thyroidectomy is performed, a patient may be able to live in a euthyroid state without the need for additional treatment. If a patient is a candidate (small nodules without cancer and a healthy BMI) endoscopic or robotic surgery is preferred. With these types of procedures, the patient has a faster healing time with smaller incisions and less postoperative pain (Kelly, 2017).

Before surgery, the patient should be treated with medications to achieve a euthyroid state. Antithyroid drugs, beta-blockers, or iodine are the most frequently used options preoperatively. The nurse should educate the patient on the potential adverse effects of these medications and when to report these to the prescribing provider (Kelly, 2017).

Postoperative complications are uncommon but may occur. According to De Leo et al. (2016), only 1-3% develop a postoperative complication. The nurse should be on alert for airway obstruction, which is a medical emergency. Laryngeal stridor may be heard due to excess edema near the surgical site. Hematoma or hemorrhage can also cause inflammation and stridor. A suction set-up and a tracheostomy kit should be readily available in the patient’s hospital room. The parathyroid glands can be accidentally removed or damaged during a thyroidectomy which can cause hypocalcemia. Severe hypocalcemia can lead to laryngeal stridor secondary to tetany, which is a series of involuntary muscle spasms. Should this occur, IV calcium gluconate should be administered to treat the tetany (Kelly, 2017).

The nurse should assess the postoperative patient every two hours for the first 24 hours. The assessment should focus on signs of hemorrhage and tracheal compression. Symptoms of this complication may include frequent swallowing, choking, bloody dressing, edema, dyspnea, or irregular breathing. The patient should remain in a semi-fowlers position while the head and neck should be supported with pillows. There should be no tension on the suture lines. Vital signs and calcium levels are monitored frequently. The nurse should monitor for signs of hypocalcemia. A positive Trousseau’s or Chvostek’s sign could be indicative of low calcium along with tingling around the mouth or extremities and muscle twitching. A positive Trousseau's sign occurs when a blood pressure cuff is inflated higher that the systolic pressure and the patient develops carpopedal spasms. A positive Chvostek's sign occurs when the cheek (area of facial nerve) is tapped, and the facial muscles twitch. If the patient has no complications, they are usually up walking within a few hours postoperatively. Oral fluids are typically allowed as tolerated. A soft diet usually begins the day after surgery (Kelly, 2017).

Once a patient is discharged following a thyroidectomy, they will need follow-up appointments to monitor thyroid function. The nurse should review with the patient the clinical manifestations of hypothyroidism and when to report symptoms to their health care provider. Caloric intake should be monitored to prevent weight gain. Education should be provided on appropriate iodine intake. Eating a serving of seafood once a week or regular use of iodized salt is often sufficient. Regular exercise is also essential to stimulate the thyroid gland (Kelly, 2017).

Future research/directions 

Over the past century, thyroid disorders have been researched with great results. One of the most beneficial research studies found that patients with hypothyroidism were being overtreated. According to McAninch and Bianco (2016), early research trials proved dosing needs for thyroid replacement therapy. Several patients in early trials were given large amounts of replacement therapy and had many adverse effects, including angina and psychosis. Dose reductions corrected those adverse effects (McAninch & Bianco, 2016).

According to the American Thyroid Association (n.d.), thyroid research funding has not increased in the last 20 years. They have 1,350 members who are dedicated to thyroid research and have young investors who perform science investigations that give promising guidance and merit for the future (American Thyroid Association, n.d.). 

References

American Thyroid Association. (n.d.). Thyroid Information. Retrieved July 15, 2019 from https://www.thyroid.org/thyroid-information/

Chaker, L., Bianco, A. C., Jonklaas, J., & Peeters, R. P. (2017). Hypothyroidism. The Lancet, 390, 1550-1562. doi: 10.1016/s0140-6736(17)30703-1.

De Leo, S., Lee, S. Y., & Braverman, L. E. (2016). Hyperthyroidism. Lancet, 388, 906-918. doi: 10.1016/s0140-6736(16)00278-6.

How does the thyroid gland work? (2018, April 19). Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK279388/

Kelly, K. A. (2017). Endocrine Problems. In Medical Surgical Nursing Assessment and Management of Clinical Problems (10th ed., pp. 1162-1171). St. Louis, MO: Elsevier.

Ledesma, C., & Lawson, S. (2018). Hashimoto's Thyroiditis. Journal of Continuing Education Topics & Review, 20(3), 86-89. 

McAninch, E. A., MD, & Bianco, A. C., MD, PhD. (2016). Correction: History and future of treatment of hypothyroidism. Annals of Internal Medicine, 164(5), 376. doi: 10.7326/m15-1799.

National Health Service. (2016). Exophthalmos. Retrieved from https://www.nhs.uk/conditions/bulging-eyes/

National Institute of Diabetes and Digestive and Kidney Diseases. (2017). Hashimoto’s Disease. Retrieved from https://www.niddk.nih.gov/health-information/endocrine-diseases/hashimotos-disease

Ross, D. S. (2018). Amiodarone and thyroid dysfunction. Retrieved from https://www.uptodate.com/contents/amiodarone-and-thyroid-dysfunction

Skidmore-Roth, L. (2015). Mosby’s Drug Guide for Nursing Students. St. Louis, MO: Elsevier/ Mosby.

Surks, M. I. (2019). Lithium and the thyroid. Retrieved from https://www.uptodate.com/contents/lithium-and-the-thyroid

Taylor, P. N., Albrecht, D., Scholz, A., Gutierrez-Buey, G., Lazarus, J. H., Dayan, C. M., & Okosieme, O. E. (2018). Global epidemiology of hyperthyroidism and hypothyroidism. Nature Reviews Endocrinology, 14(5), 301–316. doi: 10.1038/nrendo.2018.18

Wong, K. K., Shulkin, B. L., Gross, M. D., & Avram, A. M. (2018). Efficacy of radioactive iodine treatment of graves’ hyperthyroidism using a single calculated 131I dose. Clinical Diabetes and Endocrinology, 4(1). doi: 10.1186/s40842-018-0071-6