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The thyroid gland is a bilobed structure located in the anterior aspect of the trachea between the cricoid cartilage and the suprasternal notch. Each lobe of the thyroid connects via a thyroid isthmus. It is supplied via the superior thyroid artery, which stems from the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk. The term "hyperthyroidism" defines a syndrome associated with excess thyroid hormone production. It is a common misconception that the terms thyrotoxicosis and hyperthyroidism are synonyms of one another. The term "thyrotoxicosis" refers to a state of excess thyroid hormone exposure to tissues. Although hyperthyroidism can lead to thyrotoxicosis and can be used interchangeably, it is important to note the difference between them. This activity reviews the etiology, presentation, evaluation, and management of hyperthyroidism and reviews the role of the interprofessional team in evaluating, diagnosing, and managing the condition.


  • Review the various etiologies that lead to a presentation of hyperthyroidism.
  • Describe the presentation and expected examination findings when evaluating a patient with hyperthyroidism.
  • Summarize the various treatment options available for hyperthyroidism, depending on specific etiology.
  • Explain the importance of interprofessional team strategies for improving care coordination and communication to aid in prompt diagnosis of hyperthyroidism and improving outcomes in patients diagnosed with the condition.


The thyroid gland is a bilobed structure located in the anterior aspect of the trachea between the cricoid cartilage and the suprasternal notch. Each lobe of the thyroid connects via a thyroid isthmus. It is supplied via the superior thyroid artery, which stems from the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk.

Histologically, the thyroid gland is surrounded by a thin, connective tissue covering that penetrates the gland and divides the thyroid gland into compartments. The thyroid gland is composed of spherical, polarized follicular cells that surround a gel-like thyroglobulin-rich colloid. Thyroglobulin is the organic precursor for thyroid hormones and requires iodide to form thyroid hormone. Dietary iodine is transported into thyroid follicular cells via the sodium-iodide symporter after conversion to iodide via thyroid peroxidase enzyme. The process of iodide becoming incorporated into monoiodotyrosine (MIT) or diiodotyrosine (DIT) molecules is referred to as organification, and the process is relatively self-regulated. Low dietary iodide facilitated upregulation of the sodium-iodide symporter while high dietary iodide temporarily inhibits the organification process, a phenomenon known as the Wolff-Chaikoff effect.[1] Iodide incorporation into the thyroid hormone precursors, MIT and DIT, is due to the peroxidase enzyme. The organic coupling of one molecule of MIT with one molecule of DIT leads to the production of triiodothyronine (T3), while the coupling of 2 DIT molecules leads to thyroxine (T4).

The thyroid gland secretes thyroxine (T4) in response to thyroid-stimulating hormone (TSH) originating from the anterior pituitary gland. The secreted T4 is converted to a more potent and triiodothyronine (T3) via deiodinase enzymes. Most of the conversion of T4 to T3 takes place outside the thyroid, although the thyroid gland possesses the intrinsic ability for T3 production.

From a physiologic perspective, the hypothalamus releases thyrotropin-releasing hormone (TRH) in response to low circulating thyroid stimulating hormone (TSH), T3, or T4.  TRH promotes anterior pituitary secretion of thyroid-stimulating hormone (TSH), which, in turn, promotes T4 secretion from the thyroid gland. T4 and T3 exert negative feedback control on both the hypothalamus and the anterior pituitary.

The term "hyperthyroidism" defines a syndrome associated with excess thyroid hormone production. It is a common misconception that the terms thyrotoxicosis and hyperthyroidism are synonyms of one another. The term "thyrotoxicosis" refers to a state of excess thyroid hormone exposure to tissues.  Although hyperthyroidism can lead to thyrotoxicosis and can be used interchangeably, it is important to note the difference between them.


In the United States and most western countries, Graves disease is the most common cause of hyperthyroidism. As Graves disease is autoimmune in etiology, this form of hyperthyroidism tends to manifest itself in younger populations. In the older demographic, toxic multinodular goiter is the most common cause of hyperthyroidism.

Although Graves disease and toxic multinodular goiter are the more common causes of hyperthyroidism, other causes of hyperthyroidism include iodine-induced hyperthyroidism (Jod-Basedow phenomenon), thyroid adenomas, de Quervain thyroiditis (subacute thyroiditis), postpartum thyroiditis, and factitious thyroiditis (thyrotoxicosis factitia).

Factitious thyroiditis is hyperthyroidism that is associated with inappropriate or excessive use of pharmaceutical thyroid hormone. Due to a well-received side effect of weight loss, thyroxine has the potential for abuse, and any history of a hyperthyroid patient should include a medication list and an assessment of possible misuse (whether intentional or unintentional).

Other sources of hyperthyroidism include ectopic foci of thyroxine-secreting tissue. The more prevalent (although rare) form of this etiology is struma ovarii, consisting of ectopic and functional thyroid tissue (often compromising greater than 50% of total mass) in the ovary.

Amiodarone or other iodine-containing medications can induce iodine-associated hyperthyroidism or thyrotoxicosis. This iodine-induced hyperthyroidism is referred to as the Jod-Basedow phenomena (Jod is the German word for iodine).[2]


The prevalence of hyperthyroidism is different according to the ethnic group, while in Europe, the frequency is affected by dietary intake of Iodine, and some cases are due to autoimmune disease. Subclinical hyperthyroidism occurs more in women older than 65 than in men, while overt hyperthyroidism rates are 0.4 per 1000 women and 0.1 per 1000 men and vary with age. 

Any analysis of the global epidemiology of hyperthyroidism will delineate along the lines of iodine-sufficient regions and iodine-deficient regions.[3] While iodine excess can lead to hyperthyroidism, iodine deficiency can lead to both hypothyroidism and hyperthyroidism.

Graves disease is typically seen in younger patients and is the most common cause of hyperthyroidism in that demographic. Toxic multifocal goiter is typically seen in older individuals and is the most common cause of hyperthyroidism in this respective demographic. Both Graves disease and toxic multifocal goiter have a female predilection and are typically seen in patients with pertinent family and personal medical histories.

The 1977 Whickham Survey was an evaluation of the spectrum of thyroid disorders in County Durham in northeastern England. Although the demographics of the Whickham Survey consisted of primary inhabitants of a community of northeastern England (and hence, poor extrapolation potential), the survey did show interesting results of hyperthyroidism. The Whickham Survey demonstrated a prevalence of hyperthyroidism in women approximately 10-times more than that of men (2.7% versus 0.23%).[4]


The pathophysiology of hyperthyroidism depends on the particular variant of hyperthyroidism. In the case of Graves disease, the underlying cause is autoimmune, particularly the production of thyroid-stimulating immunoglobulins that bind to the TSH receptor and mimic the effects of TSH. Graves disease presents with 2 extra-thyroidal signs that are not typically seen in other forms of hyperthyroidism. The ophthalmopathy of Graves disease is characterized by the edema of retro-orbital tissues, thus causing anterior protrusion of the ocular globes. Pretibial myxedema is a plaque-like thickening of the skin anterior to the tibia due to infiltration of glycosaminoglycans in the dermis.[5]

Toxic multinodular goiter presents with palpable thyroid nodules. It is the leading cause of hyperthyroidism, particularly in older populations. Toxic multinodular goiter leads to the production of excess thyroid hormone from autonomous ectopic tissue, thus leading to clinical thyrotoxicosis.

As opposed to toxic multinodular goiter, which can present with multiple nodules, thyroid adenoma typically presents with a solitary papillary nodule that has the potential of causing hyperthyroidism. Hyperfunctioning thyroid adenomas can be distinguished from thyroid carcinomas by their clinical presentation. Thyroid hormone production by thyroid carcinomas is insufficient and cannot achieve thyroid hormone levels sufficient to cause overt hyperthyroidism. As a result, thyroid adenomas are generally benign.

Hyperthyroidism secondary to thyroiditis results in the transient increase in circulating thyroid hormone resulting from mechanical disruption of thyroid follicles. Subacute thyroiditis (De Quervain thyroiditis) typically follows an acute infection, for example, an upper respiratory infection. It is a granulomatous inflammatory process, resulting in an exquisitely tender thyroid gland. Painless thyroiditis is a form of hyperthyroidism, usually seen in postpartum stages. It is lymphocytic thyroiditis, and it can be distinguished from its subacute counterpart by the clinical history and palpation of the thyroid gland (which is non-tender in painless thyroiditis but painful in subacute thyroiditis).

Iodine-induced hyperthyroidism (Jod-Basedow phenomenon) is typically iatrogenic, resulting from the administration of iodine-containing medications such as contrast media or amiodarone. As mentioned previously, the organification of iodide residues into precursor thyroid hormone molecules is relatively self-regulating. Excessive circulating iodide inhibits organification, a process known as the Wolff-Chaikoff effect. However, professionals believe that in patients with iodine-induced hyperthyroidism, areas of autonomous function permit excessive secretion of thyroid hormone in the presence of high iodide levels. Discontinuation of the offending agent typically results in the resolution of hyperthyroidism. Amiodarone-induced thyrotoxicosis has two types: type 1 and type 2. The distinction between the 2 subtypes is apparent from history, diagnostic findings, and treatment. Amiodarone-induced thyrotoxicosis, type 1 patients typically have pre-existing thyroid pathology, low RAI uptake, and increased thyroid parenchymal blood flow. The treatment is typically anti-thyroid medication. In contrast, amiodarone-induced thyrotoxicosis, type 2 patients may not have a history of previous thyroid disease. Diagnostics may show a relatively lower RAI uptake and decreased thyroid parenchymal blood flow. Treatment for the type 2 variant is typically steroids. While excess iodine exposure from amiodarone administration can result in hyperthyroidism, amiodarone itself can be directly cytotoxic, contributing to thyroid injury.[6]

Excessively high levels of chorionic gonadotropin, as seen in cases of trophoblastic tumors, can cause hyperthyroidism via weak activation of the TSH receptors. This etiology of hyperthyroidism, however, is considerably rare compared to the previously mentioned causes of hyperthyroidism.

History and Physical

Hyperthyroidism may manifest as weight loss despite an increased appetite, palpitation, nervousness, tremors, dyspnea, fatigability, diarrhea or increased GI motility, muscle weakness, heat intolerance, and diaphoresis. The signs and symptoms of thyroid hormone exposure to peripheral tissues reflect a hypermetabolic state. A patient with hyperthyroidism classically presents with signs and symptoms that reflect this state of increased metabolic activity. Common symptoms that a patient may report include unintentional weight loss despite unchanged oral intake, palpitations, diarrhea or increased frequency of bowel movements, heat intolerance, diaphoresis, and/or menstrual irregularities.

Physical examination of the thyroid may or may not reveal an enlarged thyroid (referred to as goiter). The thyroid may be diffusely enlarged, or one or more nodules may be palpated. The thyroid may be painless to palpation or extremely tender to even light palpation.[7]


Thyroid stimulating hormone (TSH) is the initial diagnostic test of choice and is considered the best screening test for assessing the pathology of the thyroid and for the monitoring of thyroid replacement therapy. Due to the negative feedback that T3 and T4 exert on the pituitary gland, elevated T3 and/or elevated T4 will cause decreased TSH production from the anterior pituitary gland. Abnormal TSH is often followed up with a measurement of free T4 and/or free T3.[5] Concerns for an autoimmune process such as Graves disease will warrant further evaluation by assessing serum levels of TSH-receptor antibodies.[8]

TSH levels in the context of acute illness should be interpreted with more discretion as TSH levels are considerably more susceptible to the effects of illness.

Hyperthyroidism is a common etiology for atrial fibrillation; thus, further workup with an ECG may be warranted, especially in a patient complaining of palpitations. Obtaining troponin levels is not routine unless the clinical presentation warrants further cardiac ischemic workup, such as active chest pain.

Radiological diagnostics such as chest x-rays serve little diagnostic utility in the management of hyperthyroidism. Diagnostics such as ultrasound are not useful in diagnosing hyperthyroidism, but the ultrasound findings of nodules could potentially determine an etiology.

Since a majority of cases of hyperthyroidism are due to Graves disease or toxic multinodular goiter, confirmation of the diagnosis can be made based on history, clinical findings, and palpating of the thyroid. In cases of diffuse goiter or no thyroid enlargement, a 24-hour radioactive iodine uptake (RAIU) is needed to distinguish between Graves disease and other hyperthyroidism etiologies. Radioactive iodine uptake is the percentage of iodine-131 retained by the thyroid after 24 hours. For the typical western diet, the normal range of RAIU is typically 10% to 30%.

Graves disease, toxic multinodular goiter, and thyroid adenoma are etiologies of hyperthyroidism with increased RAIU, reflecting an increased synthesis of thyroid hormone. Subacute thyroiditis, painless thyroiditis, iodine-induced hyperthyroidism, and factitious hyperthyroidism have decreased RAIU. Thyroiditis represents a disruption of the thyroid follicles with the subsequent release of thyroid hormone. Since there is no increased synthesis of thyroid hormone, RAIU will be low in thyroiditis.[9]

If RAIU is not available or is contraindicated, then measurement of thyroid receptor antibodies can be used as an alternative test for diagnosis of Graves disease.[10]

A radioisotope thyroid scan is a diagnostic tool that utilizes technetium-99m pertechnetate as a radioactive tracer. The technetium-99m pertechnetate is taken up by the thyroid gland by the sodium-iodide symporter. The scan itself assesses the functional activity of thyroid nodules, classifying them as either "cold" (hypofunctioning), "warm" (isofunctioning), or "hot" (hyperfunctioning). "Cold" nodules raise concern for potential malignancy due to ineffective uptake of iodide and synthesis of thyroid hormone typically seen in thyroid carcinomas.

Treatment / Management

Treatment of hyperthyroidism depends on the underlying etiology and can be divided into 2 categories: symptomatic therapy and definitive therapy. The symptoms of hyperthyroidism, such as palpitations, anxiety, and tremor, can be controlled with a beta-adrenergic antagonist such as atenolol. Calcium channel blockers, such as verapamil, can be used as second-line therapy for patients who are beta-blocker intolerant or have contraindications to beta-blocker therapy.[11]

Transient forms of hyperthyroidism such as subacute thyroiditis or postpartum thyroiditis should be managed with symptomatic therapy alone as the hyperthyroidism in these clinical situations tends to be self-limiting.

There are 3 definitive treatments of hyperthyroidism, all of which predispose the patient to potential long-term hypothyroidism: radioactive iodine therapy (RAI), thionamide therapy, and subtotal thyroidectomy. Clinical assessment and monitoring of free T4 are imperative for patients who undergo any of these treatments. TSH-monitoring status after definitive therapy is of poor utility since TSH remains suppressed until the patient becomes euthyroid. Thus, TSH monitoring for thyroid status is not recommended immediately following definitive therapy.

The choice of which definitive treatment modality depends on the etiology. RAI therapy is considered the treatment of choice in almost all patients with Graves disease due to a high efficacy. Despite the relative safety and high efficacy, RAI is contraindicated in patients who are pregnant or patients who are breastfeeding.

In RAI therapy, radioactive iodine-131 is administered with subsequent destruction of thyroid tissue. A single dose is sufficient to control hyperthyroidism in a significant portion of patients, and the effects of other parts of the human body are essentially negligible due to the high thyroid uptake of the radioactive iodine-131. In a female patient of reproductive potential, it is highly recommended to obtain a beta-hCG to rule out pregnancy prior to initiation of RAI therapy. Any patient on a thionamide (methimazole or propylthiouracil) should be instructed to discontinue this therapy approximately 1 week prior to RAI therapy since thionamide administration can interfere with the therapeutic benefit of RAI therapy. Several months are typically needed status post-RAI therapy to achieve euthyroid status. Typically, patients are evaluated in 4 to 6-week intervals with increased time intervals for stable, plasma-free T4 levels. Failure to achieve euthyroidism after RAI therapy may indicate the need for either repeat RAI therapy (for symptomatic hyperthyroidism) or the initiation of thyroxine therapy (for hypothyroidism).

RAI therapy involves the release of stored thyroid hormone, leading to transient hyperthyroidism. This is generally well tolerated, although this transient hyperthyroidism is of concern in patients with significant cardiac disease. For patients with cardiac disease, pretreatment with a thionamide to deplete the stored hormone is recommended to avoid the potential exacerbation of cardiac disease.

Thionamide therapy is used as a definitive treatment for hyperthyroidism inpatient unwilling to undergo RAI therapy or have contraindications to RAI therapy, for example, allergy or pregnancy. Methimazole and propylthiouracil both inhibit thyroid hormone synthesis by thyroid peroxidase. Thyroid peroxidase is the enzyme responsible for the conversion of dietary iodine into iodide. Propylthiouracil (PTU) also lowers peripheral tissue exposure to active thyroid hormone by blocking the extrathyroidal conversion of T4 to T3. Thionamide therapy has no permanent effect on thyroid function, and remission of hyperthyroidism is common in patients who discontinue thionamide therapy.

The establishment of a euthyroid status typically requires several months after initiation of thionamide therapy. Although methimazole and PTU are equally effective, methimazole is preferred due to a relatively better safety profile. An exception to this recommendation is in pregnant patients, in which PTU is preferred. Methimazole is associated with an increased risk of congenital defects, and thus PTU is preferred in the management of gestational hyperthyroidism.

Side effects of thionamide therapy include agranulocytosis, hepatitis, vasculitis, and drug-induced lupus. Although these are rare side effects, patients should be warned about the potential for these side effects. Patients should also be advised to discontinue the thionamide immediately and notify their physician if symptoms suggestive of agranulocytosis occur (fever, chills, rapidly progressive infection, sore throat, among others). Routine monitoring of leukocyte counts is not recommended when starting a patient on a thionamide due to the rapid onset of agranulocytosis. A baseline comprehensive metabolic panel (CMP) to assess hepatic status would not be unreasonable due to the potential for hepatitis.

Subtotal thyroidectomy is utilized for long-term control of hyperthyroidism. Preparation of the patient for a subtotal thyroidectomy includes pretreatment with methimazole to achieve a nearly euthyroid status. Supersaturated potassium iodide is then added daily approximately 2 weeks before surgery and discontinued postoperatively. Alternatively, atenolol can be started 1 to 2 weeks before surgery to reduce resting heart rate. Supersaturated potassium iodide is also dosed and discontinued postoperatively. The rationale behind these management plans is to reduce complications associated with perioperative exacerbation of hyperthyroidism.

Complications of subtotal thyroidectomy include hypothyroidism due to the decreased secretory potential of T4. Hypothyroidism remains the most common complication associated with subtotal thyroidectomy. The proximity of the parathyroid glands to the thyroid gland can result in the removal of parathyroid glands along with thyroid tissue, resulting in hypoparathyroidism. Due to the risk of iatrogenic injury to the recurrent laryngeal nerve, vocal cord paralysis is also a complication of subtotal thyroidectomy. All of these complications should be discussed with the patient, and the discussion should be documented.

Differential Diagnosis

Hyperthyroidism presents with rather nonspecific signs and symptoms such as palpitations, increased frequency of bowel movements, weight loss, among others. Other pathologies should be ruled out as possible explanations of the patient’s symptomatology.

For etiologies of hyperthyroidism, differential diagnoses can be made based on the physical findings of the thyroid gland. Palpation of a normal thyroid gland in the context of hyperthyroidism can be due to Graves disease, painless thyroiditis, or factitious hyperthyroidism (thyrotoxicosis factitia). Graves disease can also present as a non-tender, enlarged thyroid.

Palpation of a tender, enlarged thyroid may be indicative of De Quervain thyroiditis (subacute thyroiditis). Palpation of a single thyroid nodule is likely thyroid adenoma, and palpation of multiple thyroid nodules is strongly indicative of toxic multinodular goiter.

Other differential diagnoses include euthyroid hyperthyroxinemia (a condition in which serum total T4 and T3 are elevated, but the TSH level is within normal limits) and struma ovarii.

Pertinent Studies and Ongoing Trials

Some question the addition of supplemental selenium has any effect on hyperthyroidism associated with Graves disease. One 2017 double-blinded, placebo-controlled study utilized 2 treatment arms: methimazole plus 300 mcg per day of oral selenium versus methimazole plus placebo. Although the study concluded supplemental selenium did not affect response or recurrence of Graves disease,[12] the study itself lacked sufficient data to be statistically meaningful, likely due to the small sample size in both the intervention arm and the control arm. An additional 2017 study regarding the same topic of selenium as a possible adjuvant failed to show any efficacy in supplemental selenium in short-term control of hyperthyroidism.[13]


Hyperthyroidism secondary to Graves disease or toxic multinodular goiter has an overall positive prognosis due to high success rates of definitive treatment and efficacy of symptom management. As with any disease, the prognosis of particular disease pathology is patient-oriented and reflects management, response to therapy, and compliance with prescribed treatments.


Untreated or unmanaged hyperthyroidism can lead to an extreme case of hyperthyroidism referred to as thyroid storm. Reflecting the hypermetabolic state of hyperthyroidism, the patient experiencing thyroid storm will present with tachycardia, increased GI motility, diaphoresis, anxiety, and fever. Thyroid storm is a potentially life-threatening complication of hyperthyroidism, thus requiring immediate attention. Management for thyroid storm or a high degree of suspicion of thyroid storm should include thionamide therapy (methimazole or propylthiouracil). PTU, in particular, is useful due to its inhibition of peripheral T4 to T3 conversion. Beta blockade can also be utilized in symptom management.[14]

Deterrence and Patient Education

Patient education regarding hyperthyroidism is similar to other diseases. Patients should be educated on the importance of compliance with therapy and educated on the signs and symptoms of extreme hyperthyroidism (thyroid storm).

Pearls and Other Issues

Acute coronary syndrome (ACS) may be complicated with thyroid dysfunction. A recent study has shown that thyroid dysfunction is seen in up to 23.3% of patients with coronary artery disease and both overt and subclinical hyperthyroidism in 2.5%.[15]

Pregnancy and concurrent thyroid pathology can pose a medical management challenges. PTU is recommended in pregnant women presenting with hyperthyroidism due to methimazole’s association with congenital defects. Close monitoring is recommended with PTU administration as overcorrection can potentially cause fetal hypothyroidism. Thyroid hormone is particularly important due to its role in fetal neurodevelopment. Recent literature indicates that previously recommended TSH cutoffs in pregnant women lead to overcorrection of thyroid disease in pregnant patients.[16] As fetal exposure to thyroid hormone plays a significant role, careful monitoring and close supervision are warranted.

Neonatal thyrotoxicosis results from fetal tissue exposure to excessive thyroid hormone. There are typically 2 variants of neonatal thyrotoxicosis: autoimmune-mediated and non-autoimmune-mediated. Autoimmune fetal hyperthyroidism involves the transplacental passage of TSH receptor-stimulating antibodies. Hyperthyroidism is typically transient as symptoms cease 5 to 6 months after birth following clearance of maternal antibodies. Non-autoimmune, fetal hyperthyroidism is associated with an activating mutation of either the TSH receptor or the GNAS gene (leading to McCune-Albright syndrome). As opposed to the autoimmune etiology, the non-autoimmune variant is permanent, long persisting after birth.[17]

Enhancing Healthcare Team Outcomes

Except for thyroid storm, hyperthyroidism in itself is rarely life-threatening but can pose a significant burden on a patient’s day-to-day routine. Hyperthyroidism can present with many symptoms and, if not managed, can lead to poor quality of life. Because there are many causes of hyperthyroidism, the condition is best managed by an interprofessional team.

The primary care providers, including the nurse practitioner, should educate patients on the importance of medication compliance. In addition, the patient should be informed by the pharmacist that certain products like contrast dyes, expectorants, food supplements, and seaweed tablets may contain high levels of iodine and interfere with therapy.

Inpatient management of a patient with hyperthyroidism does not always necessarily require consultation with an endocrinologist, but the presence of thyroid storm may warrant consultation with an endocrinologist and possible admission to the intensive care unit due to potentially life-threatening complications such as tachycardia and hypertensive crisis. Nurses involved with patient care should be vigilant about the signs and symptoms of thyroid storm.

As mentioned previously, any consideration of RAI therapy in a female of reproductive potential should follow a negative beta-hCG as pregnancy is an absolute contraindication to RAI therapy. Incorporating a mandatory pregnancy test as part of an overall care plan would help avoid potentially damaging radiation exposure.

Patients with Graves disease will need an ophthalmology consult. For those who undergo thyroidectomy, lifelong treatment with levothyroxine is required. Pharmacists are essential to review prescriptions, check for drug interactions, and patient education.

The interprofessional team must communicate with other members to ensure that the patient is receiving the current standard of care treatment.

(Click Image to Enlarge)
The Hypothalamus-Pituitary-Thyroid Axis.
The Hypothalamus-Pituitary-Thyroid Axis.
Contributed by M. Philip Mathew, DO
Article Details

Article Author

Philip Mathew

Article Author

Jasmine Gujral

Article Editor:

Prashanth Rawla


7/23/2022 6:12:58 PM

PubMed Link:


Nursing Version:

Hyperthyroidism (Nursing)



Markou K,Georgopoulos N,Kyriazopoulou V,Vagenakis AG, Iodine-Induced hypothyroidism. Thyroid : official journal of the American Thyroid Association. 2001 May     [PubMed PMID: 11396709]


Leung AM,Braverman LE, Consequences of excess iodine. Nature reviews. Endocrinology. 2014 Mar     [PubMed PMID: 24342882]


Taylor PN,Albrecht D,Scholz A,Gutierrez-Buey G,Lazarus JH,Dayan CM,Okosieme OE, Global epidemiology of hyperthyroidism and hypothyroidism. Nature reviews. Endocrinology. 2018 May     [PubMed PMID: 29569622]


Tunbridge WM,Evered DC,Hall R,Appleton D,Brewis M,Clark F,Evans JG,Young E,Bird T,Smith PA, The spectrum of thyroid disease in a community: the Whickham survey. Clinical endocrinology. 1977 Dec     [PubMed PMID: 598014]


Menconi F,Marcocci C,Marinò M, Diagnosis and classification of Graves' disease. Autoimmunity reviews. 2014 Apr-May     [PubMed PMID: 24424182]


Trohman RG,Sharma PS,McAninch EA,Bianco AC, Amiodarone and the thyroid physiology, pathophysiology, diagnosis and management. Trends in cardiovascular medicine. 2018 Sep 20     [PubMed PMID: 30309693]


De Leo S,Lee SY,Braverman LE, Hyperthyroidism. Lancet (London, England). 2016 Aug 27     [PubMed PMID: 27038492]


Kravets I, Hyperthyroidism: Diagnosis and Treatment. American family physician. 2016 Mar 1     [PubMed PMID: 26926973]


Meier DA,Kaplan MM, Radioiodine uptake and thyroid scintiscanning. Endocrinology and metabolism clinics of North America. 2001 Jun     [PubMed PMID: 11444164]


Bahn Chair RS,Burch HB,Cooper DS,Garber JR,Greenlee MC,Klein I,Laurberg P,McDougall IR,Montori VM,Rivkees SA,Ross DS,Sosa JA,Stan MN,American Thyroid Association.,American Association of Clinical Endocrinologists., Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid : official journal of the American Thyroid Association. 2011 Jun     [PubMed PMID: 21510801]


Ross DS,Burch HB,Cooper DS,Greenlee MC,Laurberg P,Maia AL,Rivkees SA,Samuels M,Sosa JA,Stan MN,Walter MA, 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid : official journal of the American Thyroid Association. 2016 Oct     [PubMed PMID: 27521067]


Kahaly GJ,Riedl M,König J,Diana T,Schomburg L, Double-Blind, Placebo-Controlled, Randomized Trial of Selenium in Graves Hyperthyroidism. The Journal of clinical endocrinology and metabolism. 2017 Nov 1     [PubMed PMID: 29092078]


Leo M,Bartalena L,Rotondo Dottore G,Piantanida E,Premoli P,Ionni I,Di Cera M,Masiello E,Sassi L,Tanda ML,Latrofa F,Vitti P,Marcocci C,Marinò M, Effects of selenium on short-term control of hyperthyroidism due to Graves' disease treated with methimazole: results of a randomized clinical trial. Journal of endocrinological investigation. 2017 Mar     [PubMed PMID: 27734319]


Chiha M,Samarasinghe S,Kabaker AS, Thyroid storm: an updated review. Journal of intensive care medicine. 2015 Mar     [PubMed PMID: 23920160]


Abdulaziz Qari F, Thyroid Hormone Profile in Patients With Acute Coronary Syndrome. Iranian Red Crescent medical journal. 2015 Jul     [PubMed PMID: 26421178]


Korevaar TIM,Medici M,Visser TJ,Peeters RP, Thyroid disease in pregnancy: new insights in diagnosis and clinical management. Nature reviews. Endocrinology. 2017 Oct     [PubMed PMID: 28776582]


Samuels SL,Namoc SM,Bauer AJ, Neonatal Thyrotoxicosis. Clinics in perinatology. 2018 Mar     [PubMed PMID: 29406005]