The thyroid gland is located in the anterior portion of the neck, inferior to the larynx. It consists of two lobes joined by an isthmus and is often described as being shaped like the letter "H" or a butterfly. Often embedded behind the four corners, or points, of the H shape are the parathyroid glands; in some cases, parathyroid glands may be found in the subglandular fat of the chest. These glands are visually indistinguishable from the surrounding thyroid tissue except by microscopic examination and are often inadvertently affected by treatments to the thyroid.

The thyroid gland operates as part of a feedback mechanism involving the hypothalamus and the pituitary gland. Using iodine originating in the diet and blood, the gland makes thyroid hormones that are critical to several bodily functions. First, the hypothalamus sends a signal to the pituitary gland through thyrotropin-releasing hormone (TRH). When the pituitary gland receives this signal, it releases thyroid-stimulating hormone (TSH) to the thyroid gland. Upon receiving TSH, the thyroid responds by releasing two hormones, thyroxine (T₄) and triiodothyronine (T₃), which then enter the bloodstream and affect the metabolism of the muscles as well as the heart, liver, and other organs. Finally, the pituitary gland monitors the level of thyroid hormone in the blood and increases or decreases the amount of TSH released, which then regulates the amount of thyroid hormone in the blood. This cycle constantly measures and redeploys hormones in response to the amounts measured [1,4].

Hypothyroidism is not a disease itself, but rather a clinical manifestation of the underproduction of thyroid hormones. There are many potential causes for this underactivity, including genetic factors, age, smoking status, congenital absence of the thyroid gland, surgical removal of the gland, pharmaceutical overtreatment of hyperthyroidism, lack of iodine in the diet, environmental issues, radiation therapy to the head or neck, and autoimmune disorders such as Hashimoto thyroiditis [2,7].

In the United States, newborns are screened at birth for the presence of congenital hypothyroidism with a simple blood test. One out of every 1,500 infants in the United States is born with this disorder, a number that has almost doubled in recent years, possibly due to an increase in congenital hypothyroidism with thyroid gland in-situ, lower TSH screening cutoffs, altered ethnicities of the screened population, and increased multiple and premature births [11,12]. Congenital hypothyroidism can also develop in children as they grow; most often, this is seen in children who have a strong family history of diabetes, rheumatoid arthritis, Down syndrome, or other autoimmune conditions. The earlier treatment is initiated for these children, the fewer problems are encountered as they grow. Adolescents are prone to developing Hashimoto thyroiditis, which may be a contributing cause of hypothyroidism [11,12].

In some cases, hypothyroidism may develop due to the excessive consumption of goitrogens, chemicals that block or interfere with the metabolism of iodine. Goitrogens are found in various concentrations in fruits and vegetables such as soybeans, peanuts, peaches, peas, strawberries, spinach, cabbage, turnips, cauliflower, sweet corn, rutabagas, radishes, and kohlrabi [7,14]. The moderate intake of goitrogen-rich foods is generally not associated with adverse effects unless depressed thyroid function is present.

Thyroid hormone replacement doses are based on laboratory testing rather than symptoms. Tablets are available in numerous strengths (i.e., 25 mcg, 50 mcg, 75 mcg, 88 mcg, 100 mcg, 112 mcg, 125 mcg, 137 mcg, 150 mcg, 175 mcg, 200 mcg, 300 mcg), and the typical initial oral dose is less than 200 mcg daily. This dose is increased by 50–100 mcg every one to four weeks until the desired result is achieved. Doses greater than 300 mcg per day are rare [14,16].

A routine screening, even in the absence of symptoms, may indicate an enlarged thyroid gland (on palpation) or laboratory blood testing may reveal abnormal results. The most specific test for the diagnosis of Hashimoto thyroiditis is a blood test to detect the presence of antibodies against thyroid peroxidase, an essential thyroid enzyme. There are some cases of the disease for which the blood tests are normal. In patients with Hashimoto thyroiditis, the TSH or thyrotropin test will have an increased level, indicating hypothyroidism. The TSH rises markedly when the thyroid gland has even a small underproduction of thyroid hormone. The free T₄ level may be low if there is a deficiency of thyroid hormone in the blood. Additionally, fine-needle aspiration of a nodule may be done as part of the diagnostic work-up for Hashimoto thyroiditis to exclude malignancy or the presence of a thyroid lymphoma in fast-growing thyroid goiters [7,19].

Myxedema is a rare, and frequently fatal, complication of hypothyroidism. It is seen most often in patients who have undiagnosed or untreated hypothyroidism. When patients with uncontrolled hypothyroidism are subjected to stress (e.g., infection, trauma, surgery, heart disease, seizures), they may develop full-blown myxedema or myxedema coma. Symptoms of this condition include facial and periorbital edema, thickened tongue, blank facial expression, and slowing of all motor activities. There are decreased respirations and possible respiratory acidosis. Vital signs show bradycardia, hypothermia, and a decrease in blood pressure; heart failure is a concern. It is important to begin treatment as soon as possible, as coma and death can occur. Treatment consists of intravenous levothyroxine with glucose and corticosteroids. Nursing management includes monitoring vital signs and urinary output, and close attention should be paid to the skin, as edema may cause tissue breakdown. Blankets may be necessary to combat a low body temperature. Because treatment includes thyroid supplements, it is important to be on the alert for manifestations of thyrotoxicosis, such as tachycardia, sweating, agitation, tremor, and palpitations [14,21].

There are several observable signs that indicate the possibility of hyperthyroidism in the patient. Respiratory system manifestations include shortness of breath and increased respiratory rate and depth. Cardiovascular system changes are typically seen with a rapid, bounding pulse and/or palpitations. In addition to an increased heart rate, there may also be an increased cardiac output with possible congestive heart failure and accompanying edema. Typically, both the systolic and diastolic blood pressures are elevated 10–15 mm Hg above the patient's known normal levels. The fluid retention and decreased urinary output that occur in patients with hypothyroidism may also be seen in patients with hyperthyroidism [22,23].

The three treatment options for hyperthyroidism are radiation, surgery, and thyroid-suppressing medication. Symptom relief is an important component of treatment. The choice of treatment depends upon the patient's age, physical condition, and severity of disease [22,23].

Thyroid eye disease (TED) is caused by inflammation of the muscles and connective tissue in the eye socket, which pushes the eyeball forward (i.e., proptosis). It most commonly occurs in patients with Graves disease [28]. Because more of the eye is exposed to the air, dryness and discomfort are common problems. Some interventions that may relieve the discomfort of mild-to-moderate TED include [7,28]:

Thyrotoxicosis, or "thyroid storm," is a serious and potentially fatal complication of hyperthyroidism. It is characterized by high body temperature, vomiting, severe tachycardia, irritability, delirium, dehydration, and an increase in clotting factor VIII. Once more common than it is today, thyrotoxicosis can be caused by serious infection, surgery, trauma, labor and delivery, pulmonary embolus, myocardial infarction, or critical metabolic problems in a patient with undiagnosed or untreated hyperthyroidism. Treatment involves addressing the precipitating condition and administering medication to treat the severe hyperthyroid state [22,24].

While imaging studies are no longer routinely used as part of the initial diagnostic evaluation of solitary thyroid nodules, nuclear imaging can be used to describe thyroid nodules as "hot" or "cold." Hot nodules are functional and produce thyroid hormone; they are almost never cancerous. A cold nodule is nonfunctional or inactive, producing little or no thyroid hormone. These nodules are malignant in approximately 5% to 8% of patients [31]. Ultrasound is highly sensitive in determining the size and number of thyroid nodules; however, it cannot reliably be used alone to distinguish between a benign and a malignant nodule. It may be helpful in some cases when it is used to guide fine-needle aspiration biopsy [31].

There are two types of goiters: endemic and sporadic. Endemic goiter is defined as thyroid enlargement that occurs in more than 10% of a population. Endemic goiters occur specifically in geographic areas known as "goiter belts," which are areas with soil and water deficient in iodine. Generally, these are areas without access to salt water and seafood; historically in the United States, the Midwest and Great Lakes regions have been considered "goiter belts." Coastal areas have a much lower incidence of goiters [10].

As discussed, most tumors (95%) that develop in the thyroid gland are benign, but a few are cancerous. Because the thyroid gland is close to the skin, tumors often appear as bumps in the neck. Malignant nodules can develop at any age, but they are most common in adults 30 to 60 years of age, with women often being diagnosed at a younger age than men [7,35]. While the majority of less aggressive histologic subtypes of thyroid cancer are more common in women than in men, the more aggressive subtypes have similar gender distribution. It is estimated that approximately 44,020 people (28,615 women and 15,405 men) will be diagnosed with thyroid cancer in 2024. The median age at diagnosis is 51 years [34]. A definitive cause of thyroid cancer has not been identified, but there are certain factors that increase the risk, including [35]:

Papillary carcinoma is the most common type of thyroid cancer, accounting for about 80% of thyroid malignancies [36]. It is also referred to as papillary thyroid cancer or papillary adenocarcinoma. It develops in the thyroid follicle cells and is very slow growing. In 10% to 20% of cases, both lobes of the thyroid gland are involved. There is a good prognosis with this particular cancer, and nearly all individuals with papillary cancer have good long-term survival [36].

Staging of thyroid cancer can help determine treatment options and predict the patient's prognosis. The American Joint Committee on Cancer (AJCC) has developed the TNM method of staging, which involves assessing three aspects of the cancer. T denotes the size of the tumor, N refers to the extent of metastasis to regional lymph nodes, and M indicates whether the cancer has metastasized to other organs (Table 2). After the TNM classification is complete, the carcinoma may be staged and prognosis estimated (Table 3, Table 4, and Table 5) [39,40,41].

Treatment of thyroid dysfunction in elderly individuals is also complicated. Older patients may metabolize thyroxine more slowly than younger patients. So, when treated for hypothyroidism, these patients may require lower initial doses. It is also recommended that therapy for older adults should be titrated slowly in order to prevent untoward effects.

As with any other diagnosis, patients with thyroid disease require education about their particular disease process and the importance of following a strict regimen of treatment, as outlined by their physician. Patients should have a good understanding of the medications taken to treat hypothyroidism/hyperthyroidism and how to take them correctly. Patients taking levothyroxine should be instructed to take the medication at the same time daily, on an empty stomach and with a full glass of water. Avoidance of antacids should be stressed. Those who are taking propylthiouracil to treat hyperthyroidism should be encouraged to be strictly compliant with their regimen. Avoidance of over-the-counter cold remedies that contain iodine will be necessary. Patients should also avoid driving or other hazardous activities until they know how concentration and alertness may be affected by the drug. Signs of overmedication should be reviewed, including the necessity of contacting a physician if signs arise. Patients who have been treated with radioactive iodine should be instructed regarding radiation precautions, including abstaining from close personal contact for one week after dosing.

For the traditional thyroidectomy patient, the caregiver should be alerted of the usual complications of any surgery, which include infection or excessive bleeding. The thyroidectomy patient is at risk for thyrotoxicosis, hypocalcemia (due to possible inadvertent removal of the parathyroid glands), respiratory obstruction, laryngeal edema, and vocal cord injury. Postoperatively, it is important to monitor vital signs and observe for bleeding. It is possible for these patients to bleed excessively, but for the blood to pool at the back of the neck, making it difficult to visualize. Also, it is recommended that a tracheotomy set, endotracheal tube, laryngoscope, and oxygen be readily available in the event that the patient develops a complication from swelling into the respiratory tract. The patient should be instructed to breathe deeply and cough, knowing that it will trigger increased pain at the surgical site. Be observant also for increased temperature or possible hypocalcemia. Observing serum calcium levels in the postoperative period is also helpful to verify parathyroid function [47].