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Detecting thyroid disease

Holcomb, Susan Simmons RN-CS, ARNP,BC, PhD

Evelyn Smith, 60, visits her health care provider complaining of depression, weight gain, and fatigue. Her last physical exam, a year ago, showed elevated blood pressure (BP) at 140/90, increased cholesterol, and a thyroid-stimulating hormone (TSH) level at the upper end of normal. Her vital signs include: pulse, 50 and regular; BP, 160/90; respirations, 12; and temperature, 97° F (36.1° C).

Jonah Voss, 56, comes to your emergency department complaining of abdominal pain, hot flashes, rapid heartbeat, and feeling as if he's going to jump out of his skin. He reports losing weight and having trouble sleeping. You notice he's extremely tremulous. You attach a cardiac monitor and begin oxygen (2 liters/minute via nasal cannula). Your assessment findings include: pulse, 130 and irregular; BP, 90/60; respirations, 24; and temperature, 101°F (38.3° C). The cardiac monitor reveals atrial fibrillation.

Ms. Smith and Mr. Voss are both experiencing thyroid dysfunction. About 10 million Americans have thyroid disease; hypothyroidism is more common than hyperthyroidism.

Genetics plays a role in thyroid disease. People with a family history of thyroid disease have an increased chance of developing it themselves. Age and sex are also factors, with most cases occurring after age 50 and women more likely than men to develop thyroid dysfunction.

Because many of hypothyroidism's manifestations—hair loss, fatigue, depression, and cholesterol problems—also are signs and symptoms of other diseases, you must assess carefully to identify thyroid dysfunction. To make sure you're on solid footing, let's start with a brief physiology review.

The hypothalamic-pituitary-thyroid axis, which controls hormone production, is a negative feedback system: The level of any hormone within the system affects all the other players. The hypothalamus secretes thyrotropin-releasing hormone to stimulate the anterior pituitary to secrete TSH, which in turn increases production of the thyroid hormones thyroxine (T4) and triiodothyronine (T3).

Thyroid-stimulating hormone is like a furnace controller. If the furnace is too cold, the body increases TSH output. If the furnace is running too hot, the body decreases TSH output.

Thyroid hormone actions fall into three main categories: effects on metabolic rate, growth, and specific body mechanisms. Thyroid function disorders are classified as primary (dysfunction occurs at the thyroid), secondary (dysfunction occurs at the pituitary gland), or tertiary (dysfunction results from problems with the hypothalamus). For information on the causes of thyroid dysfunction, see What's behind thyroid dysfunction?

Hyperthyroidism is the result of excess thyroid hormones; hypothyroidism results from insufficient levels of thyroid hormones. However, assessing signs and symptoms is just the start because many patients have atypical symptoms.

Thyroid dysfunction can be determined by serum TSH assay levels. To determine if the disease is overt or subclinical, the health care provider will measure free T4 (FT4) levels, which represent unbound T4 in the blood. (See Lab findings pointing to thyroid disease.)

Treating hypothyroidism

Patients with hypothyroidism need synthetic thyroid hormone to restore normal thyroid hormone levels. Levothyroxine dosing is based on age, weight, and cardiac status, with the norm being 75 to 100 mcg daily.

Because many drugs, including antacids and iron, interfere with levothyroxine absorption, advise your patient to take levothyroxine on an empty stomach and to consult her prescriber before taking any medication. Tell her she'll need assessment and blood monitoring every 6 to 8 weeks until her TSH level is normal and symptoms have disappeared. After that, she should undergo routine assessment and blood monitoring. Her TSH levels probably won't change or her symptoms reappear unless she changes brands of levothyroxine, stops taking the drug, or takes the drug with food. Teach her to take the drug at the same time each day, preferably before breakfast, to maintain constant hormone levels and prevent insomnia.

Make sure the patient understands that replacement therapy is lifetime therapy and shouldn't be stopped unless a prescriber orders. Advise her not to change brands or manufacturers of the drug and to contact her health care provider if she notices unusual bruising or bleeding, chest pain, palpitations, sweating, nervousness, or shortness of breath.

Teach her how to recognize the signs and symptoms of myxedema coma, a life-threatening complication of hypothyroidism (more on this later). Also teach her about the symptoms of hyperthyroidism, which may occur from too much thyroid hormone replacement therapy.

Treating hyperthyroidism

Treatment for hyperthyroidism involves antithyroid drugs, ablation therapy, or surgery. Surgery has fallen out of favor because of possible serious complications: hemorrhage, hypoparathyroidism, and vocal cord paralysis. However, surgery may still be indicated for patients who can't tolerate antithyroid drugs or aren't candidates for ablation therapy.

Ablation therapy using radioactive iodine is the gold standard for treating hyperthyroidism. Dosing is based on the patient's symptoms. Treatment objectives can include disabling the thyroid, inducing hypothyroidism, or trying to make the patient's thyroid function normal. Ablation therapy produces the fastest results and may be the preferred treatment for patients at greatest risk, especially the elderly and those with cardiac dysfunction. Radioactive iodine is contraindicated during pregnancy and breast-feeding because it may also disable the baby's thyroid gland. If a patient develops hypothyroidism after treatment, she'll need levothyroxine therapy.

Radioactive iodine causes minimal adverse reactions. However, besides inducing thyroiditis, it can also release stored thyroid hormone from the gland, increasing the risk of hyperthyroid cardiac instability.

Providers use antithyroid drugs such as methimazole (Tapazole) and propylthiouracil (PTU) to induce remission. Unfortunately, relapses are frequent. Because antithyroid drugs aren't a cure, they're generally reserved for pretreating patients who are elderly or have cardiac disease before starting radioactive iodine. These drugs lessen the chance of hyperthyroid cardiac effects such as tachycardia, palpitations, atrial fibrillation, fatigue, and weakness.

Antithyroid medications can cause severe adverse reactions, including agranulocytosis and hepatitis, and must be used with extreme caution in pregnant or nursing women.

Treatment for hyperthyroidism includes therapy with beta-blockers to decrease a rapid heart rate. Beta-blockers can also decrease the tremor associated with hyperthyroidism.

Nonselective beta-blockers may be contraindicated for patients with bronchoconstrictive respiratory disease, such as asthma; for them, the provider may prescribe calcium channel blockers instead, even though they're not always as effective.

Be sure to teach the patient about all possible adverse reactions to treatment.

Watching for life-threatening complications

Life-threatening complications—thyroid storm with hyperthyroidism and myxedema coma with hypothyroidism—can result from undiagnosed thyroid disease, incorrect treatment of thyroid disease, or a precipitating factor such as trauma, infection, or surgery. Fortunately, both thyroid storm and myxedema coma are rare.

The manifestations of thyroid storm include severe tachycardia with heart failure and shock, hyperthermia (up to 105.3° F [40.7° C]), restlessness, agitation, abdominal pain, nausea, vomiting, and coma. Diagnostic tests indicate increased free thyroxine (FT4), decreased TSH, elevated liver function tests, elevated alkaline phosphatase, and sometimes, hyperbilirubinemia.

The three goals of thyroid storm management are to induce a normal thyroid state, prevent cardiovascular collapse, and prevent excessive hyperthermia. Administer an antithyroid drug, such as propylthiouracil or methimazole, and large amounts of iodine to decrease thyroid hormone production. Also give glucocorticoids, which decrease thyroid hormone production by interfering with TSH. In some cases, the health care provider may order lithium carbonate to decrease thyroid hormone production or plasmapheresis and dialysis to remove excess thyroid hormone.

To prevent cardiovascular collapse, administer oxygen, intravenous fluids, beta-blockers (or calcium channel blockers if beta-blockers are contraindicated), and antithyroid medications. The patient may need vasopressors if her BP falls precipitously with signs and symptoms of low cardiac output.

To prevent excessive hyperthermia, use acetaminophen. Try to keep the patient from shivering, which can increase body temperature, cardiac oxygen demands, and metabolic demands even further. Salicylates, being highly protein-bound, are contraindicated because they prevent protein binding of triiodothyronine and thyroxine, which increases the availability of free thyroid hormones.

You'll need to frequently assess your patient's heart rate and rhythm, BP, temperature, and fluid intake and output. Also monitor her nutritional status.

Extreme hypothyroidism, or myxedema coma, usually affecting patients over age 60, is rare but often fatal. Seizures may be the first sign of myxedema. Other signs and symptoms include severe bradycardia, significantly delayed deep tendon reflexes, and hypothermia (91° to 95° F [32.8° to 35° C]). The patient also may have nonpitting edema, an enlarged tongue, and decreased level of consciousness.

Diagnostic studies will show decreased FT4, increased TSH, hyponatremia, respiratory acidosis, hypoxemia, hypoglycemia, and hyperlipidemia. A chest X-ray may show pleural and pericardial effusions, and the electrocardiogram may show prolonged QT intervals that may lead to torsades de pointes. Adrenal insufficiency may occur concurrently with myxedema coma.

Because phenytoin breaks down thyroid hormone, it's contraindicated for a patient who has seizures caused by myxedema coma; so are opioids and other drugs that depress respiration. Treatment goals are to normalize the patient's temperature, stabilize her cardiac status, and improve ventilation. Administer thyroid hormone and gradually rewarm the patient. (Reversing hypothermia will help improve cardiac and respiratory function.) Correct serum electrolyte and glucose abnormalities and start advanced cardiac life support if she develops torsades de pointes.

Administer oxygen and ventilatory support if indicated.

Screening for thyroid disease

Acting like a detective will help you detect thyroid disease. Some experts advocate screening TSH levels in all patients, especially in women, at 45 to 50 years old. Others advocate home thyroid assessment, which involves teaching patients to watch the thyroid gland's movements in the mirror as they swallow a glass of water. Patients should follow up with their health care provider if they notice any asymmetry of size or movement. Suspect subclinical hypothyroidism if a patient has signs and symptoms of hypothyroidism, such as mild depression, hypercholesterolemia, fatigue, and high-normal TSH. In cases like this, bringing her back in 6 months to remeasure the TSH level may reveal overt hypothyroidism.

Ms. Smith, one of the case patients described earlier, was diagnosed with hypothyroidism and treated with levothyroxine; her depression and fatigue improved within the first month of treatment.

Mr. Voss, the other case patient, had signs and symptoms of impending thyroid storm, and was admitted to the intensive care unit. He had ablation therapy, and a cardiologist ordered therapy to manage his atrial fibrillation and cardiac symptoms.

When you consider the prevalence of thyroid disease, extra measures to identify thyroid dysfunction early seem reasonable.

Susan Simmons Holcomb is a nurse practitioner and nutritionist working at Sastun Center of Integrative Health Care in Mission, Kan., and Olathe (Kan.) Medical Services, Inc.

The author has disclosed that she has no significant relationship with or financial interest in any commercial companies that pertain to this educational activity.

Updated from articles previously published in Nursing2003, August and September.


American Thyroid Association

Last accessed on August 10, 2005.

What's behind thyroid dysfunction?



  • Toxic diffuse goiter (Graves' disease, an autoimmune disease)
  • Toxic adenoma—more common in elderly
  • Toxic multinodular goiter—more common in elderly
  • Painful subacute thyroiditis
  • Silent thyroiditis—lymphocytic and postpartum
  • Excessive iodine intake
  • Excessive thyroid hormone replacement therapy

Signs and symptoms

  • Weight loss
  • Central nervous system (CNS): nervousness, irritability, insomnia, heat intolerance
  • Eyes, ears, nose, and throat (EENT): bulging eyes (exothalamus), unblinking stare, lid lag or retraction, goiter, hoarseness or deepening of voice (related to goiter), dry or sore throat (related to goiter), difficulty swallowing (related to goiter)
  • Musculoskeletal: tremors, fatigue, muscle weakness with muscle wasting, early or worsening osteoporosis, hyperreflexia, pretibial nonpitting edema
  • Skin/hair: increased sweating; moist palms; hyperpigmentation; fine, silky, or thinning hair; onycholysis (irregular separation of the nail plate from the nail bed distally); ridges or thickening of nails
  • Cardiac: angina, rapid heart rate, onset of atrial fibrillation, low blood pressure (BP) related to fluid loss, potential heart failure or worsening of heart failure
  • Gastrointestinal (GI): frequent bowel movement, possible diarrhea
  • Genitourinary (GU): infertility, excessive vomiting in pregnancy, increased incidence of first-trimester miscarriage



  • Hashimoto's thyroiditis—autoimmune disease
  • Other autoimmune diseases, such as amyloidosis and scleroderma
  • Radioactive iodine thyroid gland ablation
  • External radiation of the thyroid gland
  • Total or subtotal thyroidectomy
  • Defective thyroid hormone biosynthesis
  • Iodine deficiency—about 1 mg/week of dietary iodine is needed for proper thyroid function
  • Medications—lithium has antithyroid properties, and prolonged dopamine or glucocorticoid administration can suppress thyroid-stimulating hormone secretion and hormone production

Signs and symptoms

  • Weight gain
  • CNS: depression, hypersomnia, fatigue, forgetfulness, slower thinking, inability to concentrate, cold intolerance, anxiety
  • EENT: puffy eyes, enlarged tongue, hearing impairment, goiter, hoarseness or deepening of voice (related to goiter), dry or sore throat (related to goiter), difficulty swallowing (related to goiter)
  • Musculoskeletal: muscular weakness, cramps, myalgia and joint complaints, hyporeflexia, ataxia
  • Skin/hair: dry, patchy skin; coarse or thinning hair; loss of body hair, alopecia; loss of lateral eyebrows; yellow skin; appears older than stated age; myxedema (fluid infiltration of tissues leading to “doughy” skin) (late sign)
  • Cardiac: slowed heartbeat; high BP related to fluid gain; increased cholesterol levels, triglycerides, and low-density lipoproteins; potential cardiac enlargement, pleural effusion, and ascites
  • GI: constipation
  • GU: infertility, menstrual irregularities, heavy bleeding
Lab findings pointing to thyroid disease


. Retrieved June 8, 2005 from American Association of Clinical Endocrinologists and American College of Endocrinologists. American Association of Clinical Endocrinologists Guide for Clinical Practice for Evaluation and Treatment of Hyperthyroidism and Hypothyroidism. 2002.
    Bellantone, R, et al. Video-Assisted Thyroidectomy. Journal of the American College of Surgeons. 194(5):610–614, May 2002.
    Goichot, B, et al. Amiodarone-Induced Thyroiditis. Lancet. 359(9325):2275–2277, June 29, 2002.

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    Schroeder, B. ACOG Practice Bulletin on Thyroid Disease in Pregnancy. American Family Physician. 65(10):2158–2162, May 15, 2002.
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