Management of Thyroid Disorders
After completing this continuing education article, the pharmacist should be able to:
- Understand the physiology of the hypothalamic-thyroid-pituitary axis and the importance of the thyroid hormones T3 and T4.
- Define hypothyroidism and hyperthyroidism and list common causes.
- Interpret basic laboratory thyroid function tests to determine hyperthyroidism, hypothyroidism, or euthyroidism.
- Discuss oral thyroid replacement products available for the treatment of hypothyroidism and the appropriate use of these products.
- Compare the available treatment modalities for patients with hyperthyroidism and their appropriate use.
- Decide appropriate management strategies for special populations with thyroid disorders, especially pregnant and lactating women.
Thyroid hormones are necessary for proper metabolism, growth, and homeostasis. All tissues experience an increase in oxygen consumption when stimulated by thyroid hormones, with the exceptions of the brain, testes, and spleen. Thyroid hormones stimulate carbohydrate use, glucose absorption, glycogenolysis, and gluconeogenesis. Thyroid hormones also promote the growth and maintenance of healthy, mature central nervous and skeletal systems. Under- or overactivity of the thyroid gland may negatively affect the nervous system, cardiovascular system, skeletal system, and metabolism.1
The thyroid gland is located in the neck and normally weighs 15 to 20 g. Thyroxine (T4) and triiodothyronine (T3) are the main thyroid hormones and are named according to how many iodide atoms are bound: 4 and 3, respectively. The thyroid gland produces all of the body's T4 and only about 20% of its T3. The majority of T3 is produced in the liver and the kidney by removing an iodide from the T4 structure.1 Although there is significantly less T3 in the circulation than T4, T3 is significant because it is 2 to 3 times more potent than T4. T4 and T3 are highly protein-bound in plasma. Only the small fraction of free or unbound thyroid hormones, however, exerts effects on body tissues.1,2
The production and the release of thyroid hormones are regulated by the hypothalamic-pituitary-thyroid axis. Thyrotropin-releasing hormone (TRH), manufactured in the brain's hypothalamus, promotes the synthesis and release of thyroid-stimulating hormone (TSH) from the anterior pituitary. TSH then acts on the thyroid gland, leading to the synthesis and release of thyroid hormones (T3 and T4). The axis is controlled and maintained by negative feedback from thyroid hormones at both the hypothalamic and the pituitary levels. Normally, as T4 and T3 concentrations increase, the pituitary and the hypothalamus are alerted to decrease production of TSH and TRH, thus regulating thyroid hormone production.1-3
TSH is a sensitive marker, and it remains the single best indicator of thyroid function. If the TSH level is normal, primary thyroid disease is ruled out, and no further testing generally is needed. A low TSH level is an indication of hyperthyroidism, or overactivity. A high TSH level suggests hypothyroidism, or underactivity?usually of the thyroid gland itself or of the hypothalamic-pituitary-thyroid axis.
T4 and T3 levels may be measured to confirm a diagnosis of thyroid dysfunction evidenced by an abnormal TSH level. A free serum level is more accurate in detecting thyroid activity than a total serum level, which is affected by protein binding. Free T4 and T3 levels are not influenced by the degree of protein binding, which can be affected by numerous factors (illness, genetics, medications), and they are true markers of thyroid hormones' biological activity. Free T4 levels are commonly used to distinguish between hyperthyroidism, hypothyroidism, and euthyroidism.4 Free T3 serum levels are not yet commercially available, with a rapid turnaround time, for clinical use. Total T3 levels are measured occasionally when certain conditions are suspected, but these levels may be affected by protein binding.4,5
Some patients may exhibit increased or decreased TSH levels but have normal levels of T3 and free T4. If these patients do not exhibit symptoms, they are said to have subclinical thyroid disease. There is currently much debate as to whether this condition is detrimental to a patient and whether it should be treated or simply monitored closely.6 It is important to note that, during treatment, TSH levels take up to a few months longer to stabilize than T3 and T4 levels. Thus transient TSH abnormalities during treatment should not be confused with subclinical thyroid disease.5
Screening for Thyroid Disease
In 1998, the American College of Physicians recommended the following guidelines: Women >50 years of age should have serum TSH level checked. A free thyroxine test can follow when the TSH level is <0.3 to 0.4 mU/L or >10 mU/L. Routine screening of women <50 years of age or of men is not advised due to the low prevalence of symptomatic thyroid disorder.7,8
Hypothyroidism is a very common endocrine disorder in which the thyroid gland fails to release sufficient amounts of thyroid hormones. The incidence can be as high as 18/1000 people.5 The incidence of hypothyroidism increases with age and seems to more commonly affect the female gender.1,2,5
Primary hypothyroidism, a problem with the thyroid gland itself, is the most common form of hypothyroidism. Hashimoto's thyroiditis, an autoimmune disorder, leads to tissue fibrosis in the thyroid gland, which results in a decline in thyroid hormone production. Iatrogenic hypothyroidism can occur due to thyroidectomy or the use of radioiodine (131I) and is common in patients who receive these treatments for hyperthyroidism. It also is estimated that 15% of patients treated with radiotherapy for head and neck cancer will develop hypothyroidism because the radiotherapy tends to destroy the thyroid gland. In addition, medications can inhibit the production of thyroid hormones, causing hypothyroidism, through various mechanisms (Table 1).7-9
Secondary hypothyroidism is rare and is due to dysfunction of the anterior pituitary or the hypothalamus. Hypothyroidism due to pituitary failure is uncommon but should be suspected in a patient with a low thyroxine level and low TSH levels (Table 2).1,7,10,11
Thyroid replacement therapy (Table 3) is usually lifelong. Levothyroxine sodium (T4; L-thyroxine) is the treatment of choice for hypothyroidism because it is clinically stable, is relatively inexpensive, is free of antigenicity, and has uniform potency (Table 3).12-14 The synthetic T4 is converted in the body, when needed, to the more biologically active hormone T3. The half-life of levothyroxine is approximately 7 days and may be increased in the elderly. It takes 1 month to achieve steady state in all patients. Because of the long half-life, levothyroxine may be given as a once-daily dose. Levothyroxine is to be taken 30 minutes prior to meals in order to avoid delayed absorption with fiber or bran in the diet.19 Cholestyramine resin, sucralfate, aluminum hydroxide, and ferrous sulfate also will delay the absorption of levothyroxine and should not be taken within several hours of levothyroxine ingestion.10 Coadministration of carbamazepine, phenytoin, and rifampin may induce the clearance of levothyroxine; therefore, the dose of levothyroxine may need to be increased.
Levothyroxine is manufactured in the United States under the brand names of Levo-T, Levoxyl, Synthroid, and Unithroid. Because the FDA has not established standards for equivalence among the various levothyroxine preparations, patients should be kept on the same brand of thyroid replacement. If patients are switched from one brand to another, they should be closely monitored and may need a change in their drug dosage.5,20
The average patient requires thyroid replacement in a dosage of 1.6-1.7 mcg/kg/d. Elderly patients usually require less thyroid replacement; the average dose for an elderly patient is 1 mcg/kg/d. Young patients can be initiated on a dose of 50 to 75 mcg/d.2,10 Elderly patients and patients with cardiovascular disease should be initiated at a dose of 25 mcg/d. They should be monitored closely because levothyroxine may exacerbate underlying cardiac conditions, such as arrhythmias and angina. One in 5 patients with a previous history of angina will have an exacerbation of anginal symptoms when levothyroxine treatment is initiated. Patients also have experienced myocardial infarctions with the onset of therapy. Elderly patients or patients at risk for cardiovascular disease should have their dosages increased in increments of 25 mcg/d at monthly intervals to prevent stress on the cardiovascular system.2,7,10,19-21
Thyroid Product Regulation
In 1962, levothyroxine preparations were accepted by the FDA without completion of a new drug application (NDA). As a result, manufacturers were able to alter their product formulations or excipients without FDA approval, and levothyroxine products did not have to demonstrate bioequivalence to a standard formulation. Between 1987 and 1994, there were 47 cases reported to the FDA of apparent subpotent oral levothyroxine products and 9 cases of apparent superpotent levothyroxine products. Some cases were reported when switching between different brands of levothyroxine products, and others occurred when receiving refills of the same products. Subsequently, in 1997, levothyroxine manufacturers were required to submit NDAs and to have them approved in order to have their product remain on the market. The deadline to submit an NDA was August 2000.22,23
Synthroid is the leading levothyroxine product on the market today. Despite its popularity, it has not escaped potency problems. For example, a reformulation of the product in 1984 led to patients having symptoms of thyrotoxicosis. In 1989, 1991, 1998, and 2000, the product was recalled due to subpotency. Most levothyroxine products have been recalled at some time due to stability or potency problems.
The first levothyroxine products approved after the mandated NDA submissions were Unithroid (August 2000), Levoxyl (May 2001), and Levo-T (March 2002). The FDA actually threatened to withdraw Synthroid from the market because of the manufacturer's tardiness in submitting an NDA. Synthroid attempted to gain status as Generally Recognized as Safe and Effective (GRAS/E) from the FDA instead of submitting an NDA. This attempt was quickly denied by the FDA, based on concerns about the quality of the product. Synthroid later was granted extensions for the submission process. Two years after the original deadline, Synthroid gained FDA approval following NDA submission. There were no product alterations to the Synthroid product, with the exception of easier identification, with the word ?Synthroid? on the tablet.13
Other Thyroid Products
Thyroid medications were once prepared from the thyroid glands of cows, hogs, and sheep?unlike the newer products, which are synthetic. These natural medications provided both T3 and T4. The levels of T3 and T4 varied greatly between manufacturers and different product lots. These medications were antigenic in allergic or sensitive patients. The current use of these natural products?including desiccated thyroid hormone, combinations of thyroid hormone, or T3 products?generally should be discouraged.
Armour Thyroid is an example of a thyroid medication derived from animal sources that provides both levothyroxine and liothyronine. The usual starting dose of Armour Thyroid is 30 mg/d. Every 2 to 3 weeks the medication can be titrated up by 15 mg to a maintenance dose of 60 to 120 mg/d.16
Cytomel, liothyronine, is a synthetic form of T3. Liothyronine usually is initiated at 25 mcg/d and then titrated every 1 to 2 weeks by 12.5 mcg or 25 mcg/d. The usual maintenance dose of liothyronine is 25 to 75 mcg/d. Cytomel can cause an increase in cardiac side effects due to a rapid increase in serum triiodothyronine.17
Thyrolar, liotrix, is a combination of synthetic T4 and T3 in a fixed-weight ratio of 4 parts T4 to 1 part T3. The manufacturers claim that it closely simulates the action of the thyroid, although this claim is debatable.18,24
Changes in the TSH lag behind changes in the thyroid hormone. Thus the TSH and T4 concentrations should be checked no earlier than 4 weeks after the initiation of therapy. The full effect of the levothyroxine may not occur for 6 to 8 weeks, and symptomatic relief should be evaluated at that time. Patients should continue to be checked every 6 to 8 weeks, with proper adjustments made in dosages until they are euthyroid. Then the TSH level can be checked at 6- to 12-month intervals. Once patients become euthyroid, the dose of levothyroxine does not fluctuate greatly until the age of 60 or 70. As patients age, the amount of thyroid binding and the albumin decrease, resulting in an increased amount of free, active thyroid hormones. As patients age, therefore, the levothyroxine dosage may need to be decreased by 20%.10,19
Side effects of thyroid replacement generally are due to excessive amounts of medication. Diarrhea, heat intolerance, palpitations, tremors, tachycardia, vomiting, and weight loss may indicate too much levothyroxine. Other side effects may include angina, arrhythmia, congestive heart failure, myocardial infarction, and osteoporosis.3,7
Pregnancy. Hypothyroidism in a pregnant woman leads to an increased incidence of anemia, preeclampsia, postpartum hemorrhage, spontaneous abortion, low birth weight, and possible abnormal fetal brain development. Thyroid replacement is safe during pregnancy: levothyroxine is in pregnancy category A. There also is no significant transfer of the medication into breast milk. If the patient is already receiving thyroid hormone, an increase in the levothyroxine requirement is expected during pregnancy?generally by approximately 45%.2 It is recommended that TSH and free T4 levels be checked with each trimester of pregnancy and that dosage adjustments be made to maintain the TSH in the normal range. After delivery, the dose of levothyroxine should be returned to the prepregnancy dose, and the serum TSH level should be checked at 6 to 8 weeks postpartum.2,10,24
Myxedema Coma. Myxedema coma is life-threatening and can occur in patients who have had long-standing, untreated hypothyroidism. Myxedema coma usually is precipitated by an event such as a medical illness, infection, medications, or cold weather. In this condition, altered mental status, delayed reflexes, seizure, coma, and respiratory depression are common. Low blood pressure, bradycardia, hypothermia, and features of shock also may be present. Intravenous (IV) levothyroxine should be administered in doses of 0.3 to 0.5 mg. Maintenance doses are 0.05 to 0.1 mg until the patient is able to take oral dosages. Glucocorticoids, especially IV hydrocortisone, usually are required for the resulting adrenal insufficiency. Hospitalization and supportive measures are necessary until a patient is stable.25
Hyperthyroidism is the condition in which overactivity of the thyroid gland leads to an excess of thyroid hormones T3 and T4. Hyperthyroidism is common, occurring in 2% of women and 0.2% of men.26
Approximately 60% to 80% of cases of hyperthyroidism are caused by Graves' disease, or diffuse toxic goiter, which is an autoimmune disorder in which antibodies are produced that stimulate the thyroid gland.11 Another common cause, specifically in elderly patients, is Plummer's disease, or toxic multi-nodular goiter. In Plummer's disease, multiple nodules in the thyroid gland oversecrete the thyroid hormone T3.27 Thyroiditis is a group of acute conditions that usually are caused by infection and subsequent partial or complete destruction of the thyroid gland.
Thyroiditis may result in transient, self-limiting hyperthyroidism.1,28 Medications (Table 1) can induce hyperthyroidism in patients by varying mechanisms. Excess ingestion of thyroid replacement products, such as levothyroxine, may result in hyperthyroidism, which will resolve by adjusting the dose of thyroid hormone supplementation. Cancer of the thyroid gland also may result in hyperthyroidism. Other rare causes of hyperthyroidism are listed in Table 2.
There are currently 2 antithyroid medications approved by the FDA, methimazole and propylthiouracil (PTU; Table 4). These medications are thionamides, which concentrate in the thyroid gland and inhibit thyroid hormone biosynthesis. PTU, in high doses, also inhibits the peripheral conversion of T4 to the more potent T3.26 Antithyroid medications usually are used to induce remission in patients with Graves' disease. Treatment for 1 to 2 years is best associated with a chance of remission after discontinuation of medication. Patients with hyperthyroidism from other causes, such as Plummer's disease, will not experience remission. Treatment options, such as 131I, usually are more appropriate for those individuals.5,29
Methimazole generally is the drug of choice for patients with Graves' disease because its long half-life allows once-daily dosing after euthyroidism is achieved, whereas PTU must be administered 3 times daily. Patients are initially treated with high doses of antithyroid medication, 30 mg 3 times daily of methimazole or 100 mg 3 times daily of propylthiouracil. Patients should then be monitored monthly, and their antithyroid dose should be decreased as needed to retain euthyroidism.30 Free T4 levels should initially be used to monitor euthyroidism, because TSH levels may remain undetectable for several months despite adequate antithyroid treatment. Some clinicians advocate continuing high-dose antithyroid medication throughout therapy for Graves' disease and supplementing it with exogenous levothyroxine as the patient's thyroid function decreases. It is theorized that antithyroid medications have immunosuppressive effects and that higher doses may help induce remission of Graves' disease; data, however, are conflicting.10
Adverse effects with antithyroid medications are rare but serious and include agranulocytosis, liver disease, and a lupus-like syndrome. Agranulocytosis occurs in about 3/1000 patients and may be life-threatening. It is most common during the first few months of therapy. White blood cell counts should be checked at baseline and at regular intervals. If agranulocytosis is diagnosed, patients should not receive either antithyroid medication, and another treatment modality should be considered.
Liver disease is infrequent, and routine monitoring of liver function is unnecessary. Pharmacists should inform patients that if they experience fever, sore throat, muscle aches, rash, or jaundice they should immediately contact their physician. Minor, non-life-threatening adverse effects, such as pruritus, may require a patient to switch from one antithyroid medication to another.26
Lithium carbonate has been used to block the release of thyroid hormone from the thyroid gland in patients who are intolerant of PTU or methimazole, but its use is extremely rare due to its adverse-effect profile and required monitoring. 10 Stable iodine, in high doses, also can be used to decrease the production and release of thyroid hormone through an inhibitory effect. Stable iodine can be used only on a short-term basis, however, because the thyroid gland will overcome this inhibitory effect after several weeks of therapy.10
Beta-blockers are used in hyperthyroidism to treat symptoms of anxiety, tremor, and palpitations prior to obtaining euthyroidism with other treatment modalities. Two specific beta-blockers, propranolol and nadolol, have the added benefit of inhibiting the peripheral conversion of T4 to T3. Patients with hyperthyroidism may be relatively resistant to beta-blockers and may require high doses. Beta-blockers may be tapered and discontinued when euthyroidism is obtained and symptoms resolve. Non-dihydropyridine calcium channel blockers, diltiazem and verapamil, may be considered as alternative therapy if beta-blockers are contraindicated.5,27
Radioiodine was developed as a spinoff of atomic energy research during World War II. Its relatively low-cost, convenient half-life of 8 days and its effectiveness in treating hyperthyroidism led to its widespread adoption.31 131I is effective for the treatment of hyperthyroid conditions with high uptake of radioiodine, such as Graves' disease and Plummer's disease. In the United States, 131I is currently the treatment of choice for Graves' disease, according to guidelines published by the American Association of Clinical Endocrinologists in 2002.5
Doses of 131I usually range from 185 to 555 MBq (5-15 mCi) and depend on the size of the thyroid goiter, the amount of a previous tracer dose of radioiodine 131I taken up by the thyroid, and clinician preference. Some clinicians choose to give high doses of 131I to completely ablate the thyroid, rendering the patient hypothyroid after therapy, because this procedure yields quicker resolution of hyperthyroidism and minimizes the risk of hyperthyroidism-related morbidity. Other clinicians give smaller doses of 131I initially with the hope of making patients euthyroid without making them hypothyroid. Sometimes, however, these doses are not fully effective, and therapy must be repeated.31 Patients with thyroid cancer may receive up to 100 to 150 Mci of 131I for treatment.30
The acute risk associated with 131I therapy is transient radiation-induced thyroiditis, with increased symptoms of hyperthyroidism, which usually peaks at 10 to 14 days after treatment. In elderly or cardiac patients, antithyroid medication may be administered, prior to giving 131I, to achieve euthyroidism. Medication is then stopped 3 to 5 days before 131I administration and reinitiated 3 to 5 days afterward. This procedure will decrease the risk of acute thyroiditis following 131I administration. Antithyroid medications, however, also may decrease the 1-dose cure rate of 131I through a radioprotective effect and are therefore used only in high-risk patients. Patients may receive beta-blockers before and after 131I therapy to control symptoms of hyperthyroidism. Ophthalmopathy may be exacerbated by 131I therapy. A glucocorticoid taper prior to 131I therapy, as well as smoking cessation, is recommended.31
The most common long-term effect of 131I is hypothyroidism, which occurs more commonly in patients who receive higher doses of 131I. Patients usually become hypothyroid within 3 months, although hypothyroidism may occur at any time following therapy. Levothyroxine therapy should be initiated, if necessary, and titrated to meet individual patient requirements. There is always concern about the increased long-term risk of malignancy due to radiation exposure. Extensive studies, however, have shown no indication of an increase in subsequent leukemia or thyroid cancer risk in hyperthyroid patients treated with 131I .31
131I is contraindicated during pregnancy and breast-feeding. Studies have found no increased risk of cancer, infertility, or increased incidence of congenital malformations in patients or offspring if 131I is administered at least 6 months prior to conception.31 Young tissue is more sensitive to ionizing radiation, and adverse effects are more common when children are exposed to radiation. For this reason, it was previously recommended that individuals <30 years not receive 131I. Yet, the use of 131I in patients <20 years old has become commonplace, as increasing clinical experience has not led to any adverse effects.5 A review of the experience of 131I use in 587 American children, aged 1 to 18 years, for the treatment of Graves' disease showed no serious adverse effects during a followup of 23 years.34 131I should be used with caution in very young, developing children until more definitive studies are available, because the risk of carcinogenicity may be increased.33
Patients who will receive 131I for the treatment of hyperthyroidism should be provided with certain information prior to therapy. They should be advised to consume no iodine, including seafood, and to discontinue antithyroid medications several days prior. Patients also should avoid physical contact with others, especially with pregnant women or children, for approximately a week following treatment. Women are advised not to conceive, and men are advised not to father a child, for at least 6 months after therapy.28
Patients who are allergic to seafood or organoiodine-containing medications, such as amiodarone, can safely receive 131I. There are no documented allergic reactions to 131I because it contains inorganic iodide.31
Partial or total thyroidectomy was common in the past but is rarely performed currently and generally is a last resort. Patients who may be candidates include patients with thyroid cancer, pregnant patients who cannot tolerate antithyroid medications, possibly young children, and patients with very large nodular goiters. Patients usually are rendered euthyroid prior to surgery, using antithyroid medications? including stable iodine?to decrease surgical complications. Possible longterm adverse effects are very serious and include hypothyroidism, hypoparathyroidism, and vocal cord paralysis. Surgery should be performed by a surgeon who is trained and experienced in thyroid surgical procedures.26
Pregnancy. Pregnant women with uncontrolled hyperthyroidism have an increased risk of complications, such as thyroid storm, cardiac failure, hypertension in pregnancy, low birth weight, preterm labor, and stillbirth.25 Complication rates are decreased if hyperthyroidism is well-controlled during pregnancy, and ideally a patient should be euthyroid before conception occurs.25
Antithyroid medications do cross the placenta. Both PTU and methimazole are in pregnancy category D, but they are considered safe and are the treatments of choice during pregnancy because their benefit outweighs the potential risk to the fetus. Patients with uncontrolled hyperthyroidism have a much higher risk of fetal congenital abnormalities than patients being treated with antithyroid medications. PTU generally is the preferred agent in pregnancy. Antithyroid medications should be used in the lowest possible doses during pregnancy.
Pregnancy itself may decrease the activity of the thyroid gland, and some patients may have their medication tapered and require no antithyroid medication during the third trimester. Antithyroid medication requirements will immediately increase in the postpartum period, so patients should be closely monitored. It is considered safe to breast-feed while receiving antithyroid medication therapy.25
Beta-blockers, especially propranolol, are in pregnancy category C and are considered safe for use during pregnancy. Patients with uncontrolled tremor, anxiety, or tachycardia may benefit from beta-blocker therapy.25
131I is absolutely contraindicated during pregnancy and breast-feeding because of the risk of fetal or neonatal thyroid ablation. Patients are advised to utilize appropriate birth control for at least 6 months following administration of 131I. Patients who cannot tolerate antithyroid medication during pregnancy may consider thyroidectomy as a treatment option.31
In 10% to 20% of neonates born to mothers treated for hyperthyroidism, transient hypothyroidism will occur, which should resolve by day 5 of life. In 1% to 2% of neonates, a small goiter may be present at birth, which will resolve quickly. A rare serious condition of neonatal hyperthyroidism may occur around days 7 to 10 of life, and neonates should be monitored closely during that time for signs and symptoms.31
Thyroid Crisis. Thyroid crisis, or thyroid storm, is a rare, life-threatening exacerbation of hyperthyroidism that results in approximately 30% mortality despite treatment. This condition results in fever, delirium, coma, diarrhea, vomiting, jaundice, and/or seizures. This crisis usually is brought on by surgery, illness, or 131I therapy in patients with uncontrolled hyperthyroidism. Treatment includes high doses of PTU, usually a 600-mg loading dose followed by doses of 200 to 300 mg every 6 hours, either orally, rectally, or via nasogastric tube. Patients also should receive iodine (as potassium iodide, IV sodium iodide, or iopanoic acid) 1 hour after PTU administration. This iodide helps to block thyroid hormone synthesis by inducing an adaptive blockage of further iodide uptake by the thyroid gland through the Wolff-Chaikoff effect. Patients also should receive high doses of beta-blocker therapy (IV propranolol 2-5 mg every 4 hours) to control heart rate. Hospitalization and supportive measures are necessary as well until patients are stable.26
Thyroid conditions, including hyper- and hypothyroidism, are common disorders requiring pharmacologic therapy. Pharmacists should understand these thyroid disorders and have knowledge of available therapies in order to better educate patients and to orchestrate safe, effective pharmacologic management of these disorders.
Deborah DeEugenio, PharmD: Assistant Professor, Temple University School of Pharmacy, and Clinical Pharmacist, Jefferson Antithrombotics Therapy Service at the Jefferson Heart Institute, Philadelphia, Pa
Michelle Lynn Smith, PharmD: Clinical Pharmacist, Hospice Pharmacia, a division of ExcelleRX, Philadelphia, Pa
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Management of Thyroid Disorders
(Based on the article starting on page 73.) Choose the 1 most correct answer.
1. The thyroid gland normally weighs:
- 1 to 5 g.
- 5 to 10 g.
- 10 to 15 g.
- 15 to 20 g.
2. What is the current drug of choice for the treatment of hypothyroidism?
- Thyroxine4 (T4) only
- Thyroxine3 (T3) only
- A combination of T3 and T4
- Desiccated thyroid hormone
3. Screening for thyroid disease is recommended as follows:
- For women <50 years of age.
- For women >50 years of age.
- For men <50 years of age.
- Not enough information given.
4. The total starting levothyroxine dose for an elderly patient is:
- 1 mcg/kg/d.
- 1.6 mcg/kg/d.
- 25 mcg/d.
- 50 mcg/d.
5. Armour Thyroid is composed of:
- T3 only.
- T4 only.
- T3 and T4.
- Thyroid-stimulating hormone (TSH).
6. Cytomel is composed of :
- T3 only.
- T4 only.
- T3 and T4.
7. After starting thyroid replacement, TSH levels should be measured in:
- 4 to 6 days.
- ~2 weeks.
- ~4 to 6 weeks.
- ~4 months.
8. Common adverse effects of thyroid replacement products are all of the following except:
9. Thyroid replacement therapy requirements during pregnancy are expected to:
- Be increased.
- Be decreased.
- Remain the same.
- Be irrelevant because thyroid replacement is contraindicated during pregnancy due to teratogenicity.
10. Common causes of hyperthyroidism include all of the following except:
- Graves' disease.
- Buerger's disease.
- Plummer's disease.
- Excessive use of thyroid replacement products.
11. Hyperthyroidism occurs in:
- 2% of men.
- 20% of men.
- 2% of women.
- 20% of women.
12. Thyroid hormone assists in regulating all of the following except:
- Glucose absorption and utilization.
- Growth of the nervous system.
- Cerebral oxygen consumption.
- Metabolism and homeostasis.
13. The hypothalamic-pituitary-thyroid axis is regulated by:
- TSH inducing negative feedback at the hypothalamus.
- T3 and T4 inducing negative feedback at the pituitary and the hypothalamus.
- T3 and T4 inducing negative feedback at the thyroid gland.
- Increased liver metabolism of T3 and T4.
14. A common cause of hypothyroidism is:
- Graves' disease.
- Buerger's disease.
- Excessive thyroid replacement.
- Hashimoto's thyroiditis.
15. The following are considered appropriate agents for the treatment of a pregnant patient with Graves' disease except:
- Radioiodine (131I).
16. Beta-blockers are used in the treatment of hyperthyroidism to:
- Decrease secretion of T3 and T4.
- Induce remission in patients with Graves' disease.
- Control symptoms of anxiety, tremor, and palpitations.
- Eliminate the need for antithyroid medications.
17. Adverse effects of antithyroid medications include all of the following except:
- Liver complications.
18. The most important intervention to prevent progression of ophthalmopathy associated with Graves' disease is:
- Smoking cessation.
- Antithyroid medications.
19. The antithyroid medications methimazole and propylthiouracil are most appropriate in the treatment of patients with:
- Graves' disease.
- Thyroid cancer.
20. The most common long-term effect of 131I is:
- Thyroid cancer.
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