Thyroid Monograph - FreeCE

Pharmacology in Thyroid Conditions 

Release Date: 3/13/2012 

Expiration Date: 3/13/2014 

FACULTY: 

Karla Torio, MD 

Practices General and Family Medicine and Cosmetic Surgery 

FACULTY AND ACCREDITOR DISCLOSURE 

STATEMENTS: 

Dr. Karla Torio has no actual or potential conflict of interest in relation to this program. 

ACCREDITATION STATEMENT: 

Pharmacy 

PharmCon Inc is accredited by the Accreditation Council for Pharmacy 

Education as a provider of continuing pharmacy education. 

Program No.: 0798-0000-12-024-H01-P 

Credits: 1 contact hour, 0.1 CEU 

Nursing 

Pharmaceutical Education Consultants, Inc. has been approved as a provider 

of continuing education for nurses by the Maryland Nurses Association which is 

accredited as an approver of continuing education in nursing by the American 

Nurses Credentialing Center’s Commission on Accreditation. 

Program No.: N-754 

Credits: 1 contact hour, 0.1 CEU

TARGET AUDIENCE: 

This accredited program is targeted nurses and pharmacists practicing in hospital and 

community pharmacies. Estimated time to complete this monograph and posttest is 60 

minutes. 

DISCLAIMER: 

PharmCon, Inc does not view the existence of relationships as an implication of bias or 

that the value of the material is decreased. The content of the activity was planned to be 

balanced and objective. Occasionally, authors may express opinions that represent 

their own viewpoint. Participants have an implied responsibility to use the newly 

acquired information to enhance patient outcomes and their own professional 

development. The information presented in this activity is not meant to serve as a 

guideline for patient or pharmacy management. Conclusions drawn by participants 

should be derived from objective analysis of scientific data presented from this 

monograph and other unrelated sources. 

Program Overview: 

To provide participants with an understanding of pharmacology in thyroid conditions. 

OBJECTIVES: 

After completing this program, participants will be able to: 

 

 

 

 

 

 

 

Explain the pathway of thyroid hormone synthesis as a basis in the 

understanding of the mechanism of action of the thyroid and anti-thyroid 

medications 

Explain the pathophysiology of thyroid problems 

List the different medications that are being used clinically for the treatment 

of thyroid conditions 

Describe and demonstrate the uses of the thyroid and anti-thyroid 

medications in the clinical setting 

Describe the mechanism of action of the drugs used in the treatment of 

thyroid problems 

Explain the adverse effects of the drugs used in treating thyroid problems 

Correlate the knowledge gained from this monograph in clinical practice

PHARMACOLOGY IN THYROID CONDITIONS 

I. Overview 

The thyroid gland is located on the anterior part of the neck, inferior to the thyroid 

cartilage or Adam’s apple. It consists of two lateral lobes connected by the 

isthmus which wrap around the trachea. The thyroid gland produces thyroid 

hormones which regulate metabolism and are important in regulating energy, the 

body’s use of vitamins and other hormones, and the growth and maturation of 

tissues. These hormones are thyroxime (T4), triiodothyronine (T3), and 

calcitonin. 

In order for the thyroid gland to function normally, iodide is required. This is 

absorbed from the gastrointestinal tract and 90% of it is stored in the thyroid 

gland and bound to thyroglobulin (Tg). 1 The transport of iodide into the thyroid 

follicular cells is regulated by thyroid stimulating hormone (TSH) from the pituitary 

gland. Once the iodide becomes oxidized and bound to Tg, it combines with 

tyrosine moieties to form iodotyrosinases in a single conformation called 

monoiodotyrosine (MIT) or coupled conformation called diiodotyrosine (DIT). 

When a molecule of MIT and a molecule of DIT couples, T3 is formed, while T4 

results in a coupling of two molecules of DIT. 2 T3 and T4 are both bound to Tg 

and are stored in the colloid in the center of the thyroid follicle. The majority of 

the released hormone is T4, which can be converted into T3 though deiodiination 

in the peripheral extrathyroidal tissues. 

The endocrine feedback system is composed of the hypothalamus, pituitary 

gland, and thyroid gland. This is called the hypothalamic-pituitary-thyroid axis 

and all of the components act together in the regulation of thyroid hormone 

production. Thyrotropin releasing hormone (TRH) is released from the 

hypothalamus and travels through the venous plexus of the pituitary gland, 

stimulating the release of thyroid stimulating hormone (TSH). The TSH then 

travels to the thyroid gland and stimulates thyroid gland production of thyroid 

hormones. 3 

TSH stimulates cell growth and differentiation of thyroid cells, iodine uptake, and 

release of T3 and T4 from Tg. It is the major regulator of the activity and 

production in the thyroid gland, and it has feedback mechanisms to prevent its 

over or underproduction. The release of TSH from the pituitary gland is 

stimulated by increased levels of thyrotropin releasing hormone (TRH) from the 

paraventricular nucleus of the hypothalamus and decreased levels of T3. 

Negative feedback through increased levels of thyroid hormones can also affect 

TSH by inhibiting its secretion. 

Torio-Thyroid Page 1

The thyroid gland also has its own intrinsic regulatory system. When there are 

excessive stores of dietary iodide, the thyroid gland inhibits further uptake of 

iodide into the follicular cells, hence controlling the intraglandular stores of thyroid 

hormones. The reverse occurs in cases where there is iodide deficiency. 

Physiologic Effects of Thyroid Hormones 

Metabolism: T3 and T4 stimulate metabolic activities in most tissues in 

the body, resulting in an increase in basal metabolic rate. This causes an 

increase in body heat production due to increased oxygen consumption 

and energy expenditure. Increased thyroid hormone levels stimulate fat 

mobilization, which results in increased fatty acid concentration in the 

plasma. Carbohydrate metabolism is also stimulated, causing enhanced 

activity of glucose entering the cells and increased gluconeogenesis and 

glyogenolysis which generate free glucose. 

Growth and Development: Thyroid hormones are essential for the 

normal growth and development in the fetal and neonatal brain, and in 

skeletal maturation. 4 

Calcium metabolism: Calcitonin is secreted by the C cells of 

parafollicular cells of the thyroid gland. It inhibits calcium absorption, thus 

lowering serum calcium levels. Secretion of calcitonin can be stimulated 

by increased levels of serum calcium, pentagastrin, and alcohol. 

II. Pathophysiology and Etiology 

Thyroid gland diseases can result in either an overproduction (hyperthyroidism) 

or underproduction (hypothyroidism) of thyroid hormones. 

A. Hypothyroidism 

Hypothyroidism is a common endocrine disorder mainly characterized by a 

deficiency of thyroid hormone due to insufficient amounts produced by the thyroid 

gland. It could also be due to inadequate secretion of either TRH from the 

hypothalamus or TSH from the pituitary, affecting the feedback loop, and 

therefore causing hypothyroidism. 

Normally, the thyroid gland releases 100 to 125 nmol of T4 and small amounts of 

T3 daily. T4, with a half-life of 7 to 10 days, is converted in the peripheral tissues 

to T3, which is the active form of thyroid hormone. Early on in the disease, 

compensatory mechanisms are at work in order to maintain adequate T3 levels. 

When there is a decreased production of T4, the pituitary gland compensates by 


increasing the secretion of TSH, which stimulates thyroid hypertrophy and 

hyperplasia and more T3 release. 

Primary hypothyroidism is caused by thyroid gland dysfunction and is the cause 

of more than 90% of hypothyroidism cases. One of the most common causes of 

hypothyroidism is Hashimoto’s thyroiditis. It is a condition wherein there is a 

defect in the production of thyroid hormone, leading to increased TSH, which in 

turn causes goiter or thyroid gland enlargement. This is the most common cause 

of hypothyroidism after 8 years of age. 5 Antithyroid antibodies that are present in 

patients with autoimmune diseases such as systemic lupus erythematosus, 

rheumatoid arthritis, diabetes, or Sjogren’s syndrome are being recognized by 

the body as foreign and causes a reaction, leading to the infiltration of the thyroid 

gland by lymphocytes and gradual and progressive destruction of thyroid 

tissues. 4 Another condition that could lead to hypothyroidism is a lack of thyroid 

tissue due to surgical removal or by radioactive destruction of thyroid tissue. 

Drug-induced hypothyroidism may be caused by certain medications such as 

lithium, para-aminosalicylate, sulfonamides, phenylbutazone, and amiodarone. 

Iodine deficiency or excess may also result in hypothyroidism because of the 

interference in iodide organification and thyroid hormone synthesis. 6 Congenital 

hypothyroidism, discovered during screening among newborns, occurs 

approximately once in every 4,000 live births. If left untreated, it can lead to 

growth failure and mental retardation. 7 

Secondary hypothyroidism occurs in cases of pituitary dysfunction, neoplasm, or 

infiltrative disease causing a deficiency of TSH, while tertiary hypothyroidism is 

seen in hypothalamic disease (eg, neoplasm, granuloma, or irradiation leading to 

TRH deficiency). 8 

B. Hyperthyroidism 

Hyperthyroidism is a hypermetabolic state caused by excess in the synthesis and 

secretion of thyroid hormone by the thyroid gland, which can be due to 

thyrotropic stimulus or autonomous function of thyroid tissue. 4,5 On the other 

hand, thyrotoxicosis is the clinical condition which is associated with elevated 

levels of free T4 and/ or free T3. The terms hyperthyroidism and thyrotoxicosis 

are oftentimes used interchangeably; however, hyperthyroidism pertains to the 

excess synthesis and release of thyroid hormone, while thyrotoxicosis is the 

clinical presentation resulting from it. Excess thyroid hormone can result in the 

an increase in the basal metabolic rate which is related to increased production 

of body heat and cardiovascular activity, such as increased heart rate, 

contractility, and vasodilation. 

Its prevalence is 1 in every 2000 adults. Hyperthyroidism is more common 

among females, affecting 2% of women and only 0.2% of men. 5,9 


The most common cause of hyperthyroidism, accounting for 60 to 80 percent of 

cases, is Graves’ disease. 10 This is an autoimmune disease caused by an 

antibody that binds to and activates the TSH receptor and stimulates the gland to 

synthesize and secrete excess thyroid hormone. Autonomous production of 

thyroid hormone occurs when thyrocytes function independently of TSH receptor 

activation, which could result from a benign thyroid adenoma or nodules from a 

toxic multinodular goiter. Toxic adenomas are common in younger patients and 

in iodine-deficient areas. 11 Toxic multinodular goiter (also known as Plummer 

disease) accounts for about 15 to 20 percent of hyperthyroidism cases and can 

be 10-fold more common in areas where there is iodine deficiency. 11 This also 

occurs more commonly among elderly patients with a long-standing goiter. 12 

Thyroiditis is an inflammatory condition that could cause transient excess 

secretion of thyroid hormones. This includes subacute thyroiditis (caused by a 

viral infection and may resolve within eight months), lymphocitic thyroiditis, 

postpartum thyroiditis (can occur in up to 5 to 10 percent of women 3 to 6 months 

following delivery), radiation-induced thyroiditis, and pharmacologic thyroiditis 

(precipitated by amiodarone). 13 Iodine-induced hyperthyroidism can sometimes 

occur after intake of excess iodine in the diet or exposure to radiographic 

contrast media, leading to an increase in the synthesis and release of thyroid 

hormone in individuals with iodine deficiency and in older patients with preexisting 

multi-nodular goiter. 14 Rarely, hyperthyroidism can be caused by tumors 

like metastatic thyroid cancer, an ovarian tumor called struma ovarii that 

produces thyroid hormone, and trophoblastic tumors that produce beta human 

chorionic gonadotropin (β-hCG) which could weakly activate TSH receptors. 

C. Other thyroid problems 

Thyroid nodules are common and can be seen in as many as 50 percent of all 

adults, although this condition is more common in women (6%) than in men 

(2%). 4 Most of these nodules are small and benign nodules, and only 5 percent 

of the cases represent malignancy. 

III. Clinical Features and Diagnosis 

Hypothyroidism causes a wide range of clinical presentations, from 

asymptomatic to myxedema coma, or multisystem organ failure. These 

symptoms can be due to derangements in the metabolic processes or 

myxedematous infiltration or accumulation of glucosaminoglycans in the tissue. 

In the heart, myxedematous changes can result in heart enlargement, pericardial 

effusion, and poor function (ie, decreased contractility, decreased cardiac 

output). Decreased thyroid hormones can also lead to increased levels of total 

cholesterol and low density lipoprotein (LDL) cholesterol in the bloodstream 

because of a change in metabolic clearance. An increase in insulin resistance 

may also result. In the gastrointestinal tract, decreased acid secretion, 


decreased intestinal transit, and gastric stasis can occur. There may also be 

menstrual irregularities, anovulation, delayed puberty, and infertility. 

The most common symptoms of hypothyroidism are the following: weight gain, 

cold intolerance, nonpitting edema in the skin of the hands and eyelids 

(myxedema), decreased sweating, fatigue or low energy levels, loss of appetite, 

dry skin, depression, muscle and joint pains, constipation, cognitive and memory 

impairment, weakness and numbness, fullness in the throat, and voice 

hoarseness. 5 In patients with Hashimoto’s thyroiditis, common complaints 

include painless thyroid enlargement with a feeling of fullness in the throat, low 

grade fever, sore throat, and easy fatigability. 15 

In severe cases of hypothyroidism, myxedema coma can occur particularly in 

undiagnosed or untreated patients. This is characterized by bradycardia, 

pericardial effusion, altered mental status, electrolyte imbalance (eg, 

hyponatremia, hypercarbia), and ascites. 16 

Classic symptoms of hyperthyroidism include weight loss despite a good 

appetite, palpitations, tremor, and heat intolerance. Other symptoms are the 

following: insomnia, fatigue, irritability, weakness, anxiety, dyspnea, nausea and 

vomiting. Common signs include tachycardia, hyperactivity, systolic 

hypertension, warm, moist, smooth skin, and a staring gaze with lid lag. In 

patients with Graves’ disease, the thyroid gland is usually enlarged with a smooth 

and lobulated contour. Patients with toxic nodular goiter, on the other hand, one 

or more discrete nodules may be appreciated. 

In Graves Ophthalmopathy, an autoimmune process is involved, affecting the 

orbital and periorbital tissues. It is caused by the deposition of 

glycosaminoglycans in the extraocular muscles and adipose and connective 

tissues of the retro-orbital area. This results in the activation of T cells, which 

has been thought to be mediated by the TSH receptor antigen. Clinical 

manifestations include proptosis, eyelid retraction, chemosis, edema in the 

periorbital area, and altered ocular movements. 

Thyroid storm is a rare presentation of hyperthyroidism which usually occurs in 

patients with untreated or undertreated hyperthyroidism and is precipitated by 

systemic insults (ie, trauma, surgery, severe infection, myocardial infarction, etc.) 

This is characterized by fever, severe tachycardia, delirium, vomiting, diarrhea, 

and dehydration. 17 

Thyroid nodules are usually detected incidentally on imaging procedures 

because most tend to be asymptomatic. The presence of compression 

symptoms (eg, pain or difficulty in swallowing due to esophageal compression, 

hemoptysis because of tracheal invasion, dysphonia due to encasement of the 

recurrent laryngeal nerve) or invasion into adjacent tissues may point to a 


malignant cause of the nodule. The most accurate test to confirm malignant 

disease is fine needle aspiration biopsy. 

IV. Medications 

A. Hypothyroidism 

In general, the goal of thyroid replacement therapy is to replace endogenous 

thyroid hormone production, avoid iatrogenic thyrotoxicosis, and treat systemic 

complications of severe hypothyroidism. 

1. Levothyroxine 

Levothyroxine is the treatment of choice because it is well absorbed and has a 

half-life of 7 days which allows daily dosing and steady levels of T3 and T4 being 

reached in approximately 6 weeks. 18 The starting dose should take into 

consideration factors such as age, preexisting coronary artery disease, and 

cardiac arrhythmias. A starting dose of 1.6 µg/kg/day in healthy patients is 

recommended, but in elderly patients or those with cardiac disease, it would be 

prudent to start at a dose of 25 µg to 50µg once daily. 18 

2. Liothyronine 

Liothyronine (L-triiodothyronine) is rarely used alone as thyroid hormone 

replacement because it can cause rapid increases in its concentration, which 

could be detrimental in elderly patients and those with cardiac disease. It can be 

used along with levothyroxine when levothyroxine alone does not provide relief of 

symptoms. 

3. Thyroid extract 

Thyroid extract or natural thyroid hormone is pig thyroid gland that has been 

dried and crushed in powder form. This is not a recommended thyroid hormone 

replacement because the amount of T4 and T3 can be variable and there can be 

an excess T3 in this preparation. 

B. Hyperthyroidism 

1. Propylthiouracil 

Antithyroid medications such as propylthiouracil and methimazole act 

predominantly by interfering with the organification of iodine, hence suppressing 

thyroid hormone levels. Because these agents block only the synthesis of new 

thyroid hormones, the stores of preexisting thyroid hormone within the thyroid 


gland must be exhausted first before they can be fully effective, which may take 3 

to 8 weeks in patients with Graves’ disease or toxic nodular goiter. 

Propylthiouracil (PTU) is a derivative of thiourea that inhibits extrathyroidal 

conversion of T4 to T3 and is preferred for pregnant women with hyperthyroidism 

because it does not cross the placental barrier as readily as methimazole. It is 

readily absorbed, with a serum half-life of 1 to 2 hours. Its duration of action is 

longer than the half-life and should be dosed every 6 to eight hours. Its starting 

dosage is 100 mg three times daily, with a maintaining dose of 100 to 200 mg a 

day. 19 

Patients undergoing treatment with antithyroid drugs should have their thyroid 

hormone levels reassessed every 3 to 12 weeks during dose titration to monitor 

for iatrogenic hypothyroidism. Common side effects include rashes, pruritus, 

joint pains, and fever. These can be treated symptomatically without 

discontinuing the medication, but if arthralgia occurs, it should be discontinued 

because it can be a precursor of a more serious polyarthritis syndrome. 19 

Agranulocytosis is the most serious complication and may occur in 0.1 to 0.5 

percent of patients being given antithyroid medications. 19 The risk is higher in 

20, 21, 22 

those taking propylthiouracil within the first few months of therapy. 

2. Methimazole 

Methimazole blocks the oxidation of iodine in the thyroid gland. It is the drug of 

choice in nonpregnant patients because of its affordable cost, longer half-life, and 

lower risk of hematologic adverse effects. It can be taken as a single daily dose, 

improving patients’ compliance to the medication. The starting dose is 15 to 30 

mg daily, which can be given along with a beta blocker. If the patient becomes 

clinically and biochemically euthyroid after one year of medication intake, 

methimazole can be discontinued. Relapse may occur, and is generally seen 

within a year of discontinuing the medication. If there is relapse, antithyroid 

therapy can be restarted and other options such as radioactive iodine or surgery 

is considered. 21 

3. Iodide 

Iodides block the extrathyroidal conversion of T4 to T3 and inhibit release of 

thyroid hormone. It is principally used as adjunctive therapy before emergency 

thyroid surgery, to reduce vascularity of the thyroid gland before surgery, and in 

failed therapy with beta blockers. 21 These are not used in the routine treatment 

of hyperthyroidism because it tends to paradoxically increase hormone release 

with chronic use. Organic iodide radiographic contrast agents such as iopanoic 

acid or ipodate sodium are more commonly used than inorganic iodides (eg, 

potassium iodide). Iopanoic acid causes rapid and significant inhibition of 

peripheral conversion of T4 to T3 and quickly reduces T3 levels. Potassium 


iodide (Lugol solution) contains 8 mg of iodide per drop, and is used for the 

treatment of thyroid storm for 10 to 14 days prior to thyroidectomy. 

4. Beta-adrenergic receptor blockers 

Beta blockers help to promptly alleviate the sympathomimetic manifestations of 

hyperthyroidism (eg, palpitations, anxiety, tremors, and heat intolerance) 

regardless of its underlying cause. In patients with cardiac arrhythmias like sinus 

tachycardia or atrial fibrillation with a rapid ventricular response rate, beta 

blockers can function to control the heart rate. Propanolol, a nonselective beta 

blocker, is preferred because of its direct effect on hypermetabolism and is most 

commonly used, although other beta blockers can be given. 23 Propanolol also 

partially inhibits conversion of T4 to T3 in the peripheral tissues. 4 

may be the only treatment required in patients with transient forms of 

hyperthyroidism, however, in patients with more sustained forms of 

Beta blockers 

hyperthyroidism (ie, Graves’ disease, toxic nodular goiter), definitive treatment is 

10, 20, 21, 24 

necessary. 

Propanolol dose can start at 20 to 40 mg every 8 hours and be increased 

progressively up to a maximum daily dose of 240 mg until symptoms are 

controlled. Longer-acting beta blockers such as metoprolol and atenolol can also 

be used. In cases where a short-acting parenteral agent is needed, Esmolol can 

be administered. Beta blockers should be used with caution in patients with a 

history of heart disease, obstructive pulmonary disease, asthma, or Raynaud’s 

phenomenon. 

5. Radioactive iodine therapy 

Radioactive iodine causes selective uptake and concentration in thyrocytes. 

Following oral administration, it destroys thyroid tissue, thereby controlling 

hyperthyroidism effectively. This is the treatment of choice for the majority of 

patients with Graves’ disease and toxic nodular goiter. High dose radioactive 

iodine therapy is recommended in elderly patients, those with preexisting cardiac 

disease, and patients with toxic nodular goiter or toxic adenomas. 25 

Its main adverse effect is the development of postablative hypothyroidism, which 

is more commonly seen in patients with Graves’ disease. Lifelong monitoring of 

thyroid hormone levels is necessary because patients develop this complication 

at a rate of 3% annually. Another side effect is the transient worsening of 

hyperthyroidism during the first month of treatment due to radiation thyroiditis. 

Opthalmopathy may develop or exacerbate in 15 percent of patients with Graves’ 

26, 27 

disease, especially in those who smoke cigarettes. Lower dose radioactive 

iodine or prednisone can be used in those patients to reduce the risk of 

ophthalmopathy. 28 


Radioactive iodine is contraindicated in pregnant or lactating women because it 

can readily cross the placenta barrier and can be excreted into milk. This can 

lead to an ablative effect to the infant’s thyroid gland resulting in hypothyroidism. 


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