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NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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StatPearls [Internet].


Philip Mathew ; Jasleen Kaur ; Prashanth Rawla .


Last Update: March 19, 2023 .

  • Continuing Education Activity

Hyperthyroidism is a common thyroid disorder with multiple underlying etiologies. This disease is characterized by excess thyroid hormone production. Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is defined as low or suppressed thyroid stimulating hormone (TSH) levels with elevated triiodothyronine (T3) levels and/or elevated thyroxine (T4) levels. Hyperthyroidism is associated with significant short-term and long-term morbidity. Therefore, early recognition of this condition and timely instruction of appropriate therapy is critical. 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.
  • Introduction

Hyperthyroidism is a common thyroid disorder. "Hyperthyroidism" defines a syndrome associated with excess thyroid hormone production. [1] It is a common misconception that the terms thyrotoxicosis and hyperthyroidism are synonyms. The term "thyrotoxicosis" refers to a state of excess thyroid hormone exposure to tissues. [1]  Although hyperthyroidism can lead to thyrotoxicosis and can be used interchangeably, it is essential to note their differences. For the sake of simplicity, this review will cover a discussion of hyperthyroidism and thyrotoxicosis. Hyperthyroidism has multiple etiologies, clinical manifestations, and treatment modalities.

Hyperthyroidism can be overt or subclinical. Overt hyperthyroidism is defined as low or suppressed thyroid stimulating hormone (TSH) levels with elevated triiodothyronine (T3) levels and/or elevated thyroxine (T4) levels. [1] When T3 levels are elevated with low/suppressed TSH and normal T4 levels, this is called 'T3 toxicosis'. [2] Subclinical hyperthyroidism is low or suppressed TSH with normal T3 and T4 levels. [2] Both overt and subclinical hyperthyroidism are associated with significant long-term complications. [3] [4] [5] [6] [7]

The three most common etiologies of hyperthyroidism include:

  • Graves disease (GD)
  • Toxic multinodular goiter (TMNG)
  • Toxic adenoma (TA) [1]

Other less common etiologies of hyperthyroidism:

  • Iodine-induced hyperthyroidism [8]
  • TSH (thyroid stimulating hormone)-secreting pituitary adenomas [9]
  • Conditions associated with high human chorionic gonadotrophin levels: choriocarcinomas and hydatiform moles in females and germ cell tumors in males [10]
  • Ectopic thyroid in struma ovarii (excess thyroid hormone production from ovarian teratomas) [11]
  • Extensive metastasis from functionally differentiated thyroid carcinoma (follicular or papillary) [12]
  • Drug-induced thyroiditis: amiodarone, lithium, tyrosine kinase inhibitors, interferon-alpha, immune checkpoint inhibitor therapy [13] [14] [15] [16] [17]
  • Other thyroiditis: Hashitoxicosis, painless thyroiditis, painful subacute thyroiditis, suppurative thyroiditis, and Riedel thyroiditis [18] [19]
  • Factitious thyroiditis (due to excess exogenous thyroid hormone: intentional or unintentional use) [10]

Graves disease is the most common cause of hyperthyroidism in the United States and most Western countries. [20] As Graves disease is autoimmune in etiology, this form of hyperthyroidism tends to manifest itself in younger populations. In older adults and people living in regions of iodine deficiency, toxic multinodular goiter is the most common cause of hyperthyroidism. [21] [22] [23]

Factitious thyroiditis is thyrotoxicosis associated with inappropriate or excessive use of pharmaceutical thyroid hormone. [10] Due to a well-received side effect of weight loss, thyroxine has the potential for abuse. Any history of a hyperthyroid patient should include a medication list and an assessment of possible misuse (whether intentional or unintentional).

  • Epidemiology

The prevalence of hyperthyroidism varies worldwide, based on dietary iodine content. [12]  Hyperthyroidism is more common in women compared to men. [24]  Other risk factors associated with the development of hyperthyroidism include smoking, iodine deficiency, iodine excess, selenium deficiency, genetic factors, and the use of certain drugs. [12]  Graves disease is typically seen in younger patients and is the most common cause of hyperthyroidism in this demographic. The incidence of GD is highest between the age group of 30 to 50 years. [25] Toxic multifocal goiter is typically seen in older individuals and is the most common cause of hyperthyroidism in this demographic. [22]  Graves disease and toxic multifocal goiter have a female predilection and are typically seen in patients with pertinent family and personal medical histories. Thyroid nodular disease is also more common in women than men by 5- to 15-fold. [26] Autoimmune thyroid disorders like Graves disease are more common in iodine-replete areas, and nodular thyroid diseases are more common in iodine-deficient areas. [12]

The 1977 Whickham Survey evaluated the spectrum of thyroid disorders in County Durham in northeastern England. The Whickham Survey demonstrated a prevalence of hyperthyroidism in women, approximately ten times more than that of men (2.7% versus 0.23%). [27]  An incidence of 80 cases per 100,000 women was seen at the 20-year follow-up of the Whickham cohort. [28]  The prevalence of hyperthyroidism in the United States was 1.3% in the general population, with 0.5% cases of overt hyperthyroidism and 0.7% cases of subclinical hyperthyroidism. [29]  A meta-analysis found the prevalence of hyperthyroidism in Europe to be 0.75%. [24]  The prevalence of overt hyperthyroidism is similar in China at 0.78%. [30]  

Amiodarone-induced thyrotoxicosis (AIT) is seen in about 6% of the individuals taking the medication in iodine-sufficient areas and about 10% in individuals taking the medication from iodine-deficient areas. [31] [32]

  • Pathophysiology

The pathophysiology of hyperthyroidism depends on the particular variant of hyperthyroidism.

Graves Disease

This is an autoimmune process with antibodies against the TSH receptor. An interplay between genetic and environmental factors influences this autoimmune process. The antibodies stimulate the TSH receptor (TSHR), leading to increased production and release of thyroid hormones. The trophic effects on the thyroid also lead to the growth of the thyroid gland. [20]  

Toxic Multinodular Goiter

Pathogenesis of TMNG includes the initial phase of development of the nodular disease. This phase is prolonged and present for years before the nodules develop autonomy for thyroid hormone production. The somatic mutations involving the TSHR lead to constitutive activation of the cAMP signaling pathway, resulting the thyroid autonomy. [33]  There is a correlation between the size of the nodules and the development of hyperthyroidism. In a previous study, about 93.7% of the patients who developed overt hyperthyroidism had a nodule size greater than 3 cm. [34]   

Toxic Adenoma

These are solitary nodules with autonomous thyroid hormone production due to somatic mutations in the TSHR

Iodine-Induced Hyperthyroidism (Jod-Basedow Phenomenon)

This is typically iatrogenic, resulting from excessive iodine intake through diet or administration of iodine-containing medications such as contrast media or amiodarone. [35] [36] Individuals susceptible to this phenomenon include the ones residing in iodine-deficient regions, individuals with underlying thyroid nodular disease, or underlying occult GD or previously treated GD. [8]  Hyperthyroidism develops about 2-12 weeks after exposure to excessive iodine. [37] 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. This autoregulation is escaped in the Jod-Basedow phenomenon leading to excess thyroid hormone in the presence of excess iodine/iodide.

Amiodarone-Induced Thyrotoxicosis

There are two subtypes of amiodarone-induced thyrotoxicosis (AIT): type 1 and type 2. Type 1 AIT leads to increased thyroid hormone production secondary to excess iodine exposure from amiodarone in the setting of pre-existing thyroid disease (as seen in the Jod-Basedow phenomenon). [38] The pre-existing thyroid disease is usually multinodular goiter or latent Graves disease. Type 2 AIT is destructive thyroiditis due to the direct toxic effects of amiodarone on the thyroid follicular cells. [39]

Thyroiditis results in the transient increase in circulating thyroid hormone resulting from inflammation or destruction of the thyroid follicular cells. Various etiologies of thyroiditis have this common pathophysiology but vary in their clinical presentations. The inflammation or destruction of the thyroid follicular cells can result from autoimmunity (Hashimoto's thyroiditis, painless sporadic thyroiditis, and painless postpartum thyroiditis) or the result of external factors (infections in painful subacute thyroiditis, suppurative thyroiditis, drug-induced thyroiditis). [19]

  • History and Physical

Thyroid hormone has physiological effects on multiple organ systems. As a result, the symptoms and signs of hyperthyroidism involve manifestations from multiple organ systems. Clinical manifestations are associated with a hyperadrenergic and hypermetabolic state. Common manifestations include unintentional weight loss (about 10% of patients can gain weight due to increased appetite), palpitations, tremors, heat intolerance, dyspnea on exertion, increased anxiety, irritability, fatigue, muscle weakness, increased frequency of bowel movements (some patients can have significant diarrhea), hair loss, loss of libido, and oligomenorrhea or amenorrhea in women. [20] [40]  

Patients with subacute thyroiditis can present with significant anterior neck pain and fever. On physical examination, patients have tachycardia (some can present with atrial fibrillation), hypertension, tremors, warm and moist skin, hyperreflexia, and an anxious appearance. Some patients might have signs of heart failure.

Eye signs of lid lad or lid retraction can be seen in all causes of hyperthyroidism due to a hyperadrenergic state. [41] Eye symptoms and signs of "true orbitopathy' are only seen in patients with Graves disease. These include diplopia, excessive tearing, conjunctival injection, and orbital or retro-orbital pressure proptosis. [42] [43] Other specific physical findings associated with Graves disease are pretibial myxedema (plaques of thick, scaly skin and swelling involving the anterior aspect of lower legs) and acropachy (soft-tissue swelling of the hands and clubbing of the fingers). [44] [45] [46]

Examining the thyroid will reveal a diffuse non-nodular enlargement of the thyroid in Graves disease; a diffuse non-symmetric nodular enlargement can be seen in toxic multinodular goiter, and a single large nodule can be palpated in cases of a toxic adenoma. An exquisitely tender thyroid can be noted in subacute thyroiditis. [47]  

When hyperthyroidism is suspected based on clinical features, the patient should undergo an initial evaluation with measurement of TSH, free T4, and total T3 to confirm the diagnosis. Figure 1 illustrates the diagnostic algorithm for hyperthyroidism. Patients with overt hyperthyroidism will have low/suppressed TSH levels with elevated free T4 and total T3 levels. Patients with mild/subclinical hyperthyroidism will have low/suppressed TSH with normal free T4 and total T3 levels. 'T3 toxicosis' is defined as low/suppressed TSH with normal T4 and elevated T3 levels.

Conditions that can interfere with the assessment of TSH include the presence of heterophile antibodies and high biotin intake due to interference with the assays. [48]  Heterophile antibodies can lead to a false elevation in TSH levels. High-dose biotin supplementation (5 to 30 mg) can result in falsely low TSH with elevated free T4 levels in vitro. [49]

After the diagnosis of hyperthyroidism has been confirmed, measurement of thyrotropin receptor antibody (TRAb) levels as an initial test for determining the etiology of hyperthyroidism has been shown to reduce the time to diagnosis and is more cost-effective. [50] . Elevated TRAb levels confirm the diagnosis of Graves disease. TRAb levels are measured using TBI or TBII (thyrotropin-binding inhibiting or thyrotropin-binding inhibitory immunoglobulin) assays and TSI (thyroid stimulating immunoglobulin) bioassays. The newer bioassay using the Immulite method for TSI measurement has a high sensitivity and specificity of 98% and 99.9%, respectively, for diagnosing GD. [51]  TBII assays used for measuring TRAb levels also have a high sensitivity of 96-97% and specificity of 99% of the diagnosis of GD. [52]

If TRAb levels are normal, the patient should undergo a radioiodine thyroid uptake and scan using an I-123 isotope (enters the thyroid gland through the Na/I symporter). This test is contraindicated in pregnant and lactating women. A capsule containing an I-123 isotope is given a day before the scan is performed. The pattern of uptake of I-123 by the thyroid gland seen on the scan can help determine the diagnosis (see Figure 1). However, this test does not help differentiate between type 1 and type 2 amiodarone-induced thyrotoxicosis, as the uptake will be low in chronic amiodarone use.

  • High Uptake/Normal
  • Graves disease will have high or normal uptake in a diffuse pattern
  • TMNG will have a high or normal uptake in a patch pattern
  • TA will have a high or normal uptake with a solitary area of high uptake (corresponding to the known nodule) with low uptake in the remainder of the gland
  • Low or Absent Uptake
  • Any etiology of thyroiditis is associated with low or absent uptake (Na/I symporters are not functional in inflamed or destroyed thyroid follicular cells)
  • Iatrogenic and factitious thyrotoxicosis

Thyroid ultrasound using the color Doppler is another important test that can help determine the underlying etiology. Intrathyroidal arterial flow velocities are measured. [53]  Increased (thyroid inferno) and normal flow are seen in Graves disease. Low flow is seen in thyroiditis. [53]  This test can help differentiate between type 1 and type 2 amiodarone-induced thyrotoxicosis (AIT). The flow will be high or normal in type 1 AIT (hyperthyroidism due to underlying nodular thyroid disease or occult GD) and low in type 2 AIT (destructive thyroiditis). [54]

  • Treatment / Management

Treatment of hyperthyroidism depends on the underlying etiology and can be divided into symptomatic 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 treatment. [1]

This review will only discuss the treatment for the most common causes of hyperthyroidism: Graves disease, toxic multinodular goiter, and toxic adenoma in non-pregnant patients. 

Indications for treatment:

  • Overt hyperthyroidism
  • Subclinical hyperthyroidism with TSH <0.1 and age >65 years
  • Subclinical hyperthyroidism with TSH <0.1 and age <65 years with comorbidities (cardiovascular disease, osteoporosis, or symptomatic)
  • Subclinical hyperthyroidism with TSH <0.1 and age <65 years, if TSH still elevated after 3 to 6 months
  • Subclinical hyperthyroidism with TSH between 0.1-0.4 and age >65 years, if TSH still elevated after 3 to 6 months
  • Subclinical hyperthyroidism with TSH between 0.1-0.4 and age <65 years with comorbidities (cardiovascular disease, osteoporosis, or symptomatic), if TSH still elevated after 3-6 months

There are three definitive treatments for hyperthyroidism: radioactive iodine therapy (RAI), thionamide therapy, and subtotal thyroidectomy. The choice of which definitive treatment modality depends on the etiology, comorbidities, and patient preferences. Historically, radioactive iodine (RAI) has been the preferred treatment for managing Graves disease in the United States. Still, the trend is changing towards increased use of anti-thyroidal drugs (ATD). [55]  ATDs have been the preferred treatment for Graves disease in most other countries. [1]  

Antithyroid Drugs (ATDs)

Thionamide drugs include methimazole, carbimazole (precursor of methimazole), and propylthiouracil. These drugs are competitive inhibitors of the thyroid peroxidase (TPO) enzyme, resulting in their ability to block thyroid hormone synthesis. Additionally, these drugs may have additional immunosuppressive effects, as shown by their ability to induce remission in patients with Graves disease. [56] [57]  Methimazole and propylthiouracil both inhibit thyroid hormone synthesis by thyroid peroxidase. Thyroid peroxidase is the enzyme responsible for converting 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 recurrence of hyperthyroidism is common in patients who discontinue thionamide therapy.

Attaining a euthyroid status typically requires several months after initiation of thionamide therapy. Although methimazole and PTU are equally effective, methimazole is preferred due to once-daily dosing and 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 managing hyperthyroidism during pregnancy.

  • ATA (Americal Thyroid Association) guidelines provide a rough guide for the initial dose of methimazole based on free T4 levels  [1]
  • Free T4 1-1.5 times upper limit of normal: Start methimazole 5-10 mg daily
  • Free T4 1.5-2.0 times the upper limit of normal: Start methimazole 10-20 mg daily
  • Free T4 2.0-3.0 times the upper limit of normal: Start methimazole 30-40 mg daily
  • PTU is administered in 2-3 doses per day due to its shorter duration of action. The initial dose of 5-150 three times daily is chosen based on the severity of hyperthyroidism. Once the disease is controlled, the dose can be decreased to a maintenance dose of 50 mg 2 to 3 times daily.
  • Monitoring: TSH levels remain suppressed for almost six months in patients with Graves disease, so evaluation of free T4 and/or total T3 levels should be done every 4 to 6 weeks. 
  • Pregnancy: Propylthiouracil is the preferred drug in the first trimester, associated with lower incidence and severity of embryopathy than methimazole. [58] [59]  The treatment can be switched to methimazole after 16 weeks of gestation.
  • Drug conversions:
  • 10 mg of carbimazole is converted to approximately 6 mg of methimazole  [1]
  • An equivalent dosage ratio of propylthiouracil to methimazole is 20:1. This ratio is recommended for dose conversions when switching between these agents. [60]

These drugs should be continued for at least 12-18 months. TRAb should be assessed at that time to evaluate for remission. If TRAb levels are normal, then thionamide therapy can be discontinued. If TRAb levels are still elevated, the patient remains at high risk for relapse if medication is stopped. Other factors associated with lower remission rates: male gender, smoking, large goiters, higher TRAb titers at the time of diagnosis, presence of orbitopathy, and the need for a high dose of thionamides to maintain euthyroidism. [20]

An older study from the United States showed a 20-30% remission rate for Graves disease using thionamides. [61]  European and Japanese populations noted higher remission rates of 50-60%. [62] [63] [64]

Radioactive Iodine (RAI)

RAI (using I-131 isotope) can be the preferred therapy in most patients, especially the ones with high-risk comorbidities who are at high risk for surgery and need definitive management. Patients who have contraindications for the use of thionamides should also undergo RAI. This procedure should be avoided in patients planning a pregnancy in the six months due to the risk of inducing hypothyroidism in the fetus. RAI is also contraindicated in lactating women. Patients will a history of moderate to severe Graves orbitopathy should not undergo treatment with RAI due to the risk of worsening eye disease. Patients with underlying thyroid malignancies should not undergo RAI. 

Radioactive iodine-131 leads to the destruction of thyroid follicular cells. In a female patient of reproductive age, it is highly recommended to obtain a beta-hCG to rule out pregnancy before initiation of RAI therapy. Patients on a thionamide (methimazole or propylthiouracil) should be instructed to discontinue this therapy approximately one week before 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.

  • Graves disease
  • A single fixed dose of 10-15 mCi (370-555 MBq) is sufficient to render a patient with GD hypothyroid. Doses of RAI can be calculated using the size of the thyroid gland and the uptake of RAI. Cure rates are higher with higher doses, up to 85%. [65] [66]  
  • Toxic multinodular goiter
  • A single dose of 15 mCi is usually sufficient. [67]  A calculated dose of 150-200 microCi (5.5-7.4 MBq) per gram of thyroid tissue can be used, corrected for 24-hour radioactive iodine uptake. Cure rates are 55% at three months and 80% at six months. [68]  Long-term studies have shown that the risk of hypothyroidism after RAI for TMNG is 3-5% by one year, 16% by five years, and 64% by 24 years. [69] [70] [71]
  • Toxic adenoma
  • A single fixed of 10-20 mCi (370-740 MBq) is usually sufficient. The dose can also be calculated based on nodule size: 150-200 microCi (5.5-7.5 MBq). [72]  Long-term studies have shown that the risk of hypothyroidism after RAI for TA is 8% in 1 year and 60% in 20 years. [73]

Typically, patients with GD are evaluated in 4 to 6-week intervals with an assessment of TSH, free T4, and total T3 levels. The monitoring should continue for another six months or till the patient becomes hypothyroid and is on a stable dose of levothyroxine. 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 due to the destruction of thyroid follicular cells, 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 the cardiac disease. In addition, the use of beta-blocker therapy is also essential in these patients to minimize beta-adrenergic symptoms.

Preferred in women planning a pregnancy in less than six months, presence of active Graves orbitopathy, patients who experience significant adverse effects with the use of thionamides, when thyroid malignancy is suspected, presence of large compressive goiters, and the presence of co-existing hyperparathyroidism needing surgery. The surgical option should be avoided in patients with significant comorbidities deemed high-risk for undergoing surgery.

Euthyroidism should be achieved before surgery with the use of thionamides. Preoperative SSKI (saturated solutions of potassium iodide), KI (potassium iodide), or Lugol's iodine should be used in patients with Graves disease and TMNG to decrease gland vascularity and decrease intraoperative blood loss. [74] [75]  

  • Graves disease: Near-total or total thyroidectomy is the surgical procedure of choice in patients with Graves disease, with excellent cure rates. The risk of recurrence or disease persistence with total thyroidectomy is almost 0% versus 8% with sub-total thyroidectomy after five years. [76] [77] [78]
  • Toxic multinodular goiter: Surgical option of choice is near-total or total thyroidectomy to avoid recurrences. [79] [80]
  • Toxic adenoma: Preferred surgical option is ipsilateral thyroid lobectomy or isthmusectomy, with excellent cure rates and a risk of the treatment failure rate of less than 1%. [81]

After patients undergo near-total or total thyroidectomy, they should be started on weight-based levothyroxine replacement therapy (0.8 mcg/lb or 1.6 mcg/kg). Lower doses should be used in the elderly, especially in patients with a history of cardiovascular disease or arrhythmia.

  • Differential Diagnosis

Hyperthyroidism presents with relatively nonspecific signs and symptoms such as palpitations, increased frequency of bowel movements, and weight loss, among others. Therefore, other pathologies should be ruled out as possible explanations for 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 indicate De Quervain thyroiditis (subacute thyroiditis). Palpation of a single thyroid nodule is likely indicative of thyroid adenoma, and palpation of multiple thyroid nodules strongly indicates toxic multinodular goiter.

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

  • Toxicity and Adverse Effect Management

Antithyroid drugs or thionamides are associated with rare but serious adverse effects of agranulocytosis, hepatotoxicity, and vasculitis. Hepatotoxicity is more common with the use of propylthiouracil (2.7%) than methimazole (0.4%). [82]  Hepatotoxicity due to methimazole is more likely to be cholestatic, while hepatotoxicity due to PTU is more likely to be hepatocellular. [83] Hematological complications have an incidence of 0.1-0.15% with the use of PTU or methimazole. Of these patients, 89% had agranulocytosis, and 11% had pancytopenia or aplastic anemia. [84]  Patients taking PTU and rarely methimazole can develop p-ANCA (anti-neutrophil cytoplasmic antibody) positive small vessel vasculitis. [85] Up to 40% of those taking PTU can develop c-ANCA positivity, but very few develop vasculitis. [86] [87]  These medications are also associated with the development of drug-induced lupus. [88] [89]  Few cases of hypoglycemia secondary to autoimmune insulin syndrome have been reported using methimazole. [90] [91]

If patients develop an acute febrile illness with symptoms of pharyngitis, they should get blood work done to check complete blood cell counts along with differentials to rule out the development of agranulocytosis. Liver function tests should be assessed in patients who develop a pruritic rash, abdominal pain or bloating, anorexia, nausea, vomiting, fatigue, jaundice, light-colored stool, or dark urine.

The most common complications following total or near-total thyroidectomy include hypocalcemia due to hypoparathyroidism in less than 2% of cases (can be transient or permanent), recurrent or superior laryngeal nerve paralysis in less than 2% of cases (can be temporary or permanent), hemorrhage, and complications related to anesthesia. [92] [93] [94]

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

  • Complications

Untreated or unmanaged hyperthyroidism can lead to an extreme case of hyperthyroidism, referred to as a thyroid storm. Reflecting the hypermetabolic state of hyperthyroidism, the patient experiencing thyroid storm will present with tachycardia, increased GI motility, diaphoresis, anxiety, fever, and manifestations of multiple organ dysfunction. Thyroid storm is a potentially life-threatening complication of hyperthyroidism, thus requiring immediate attention. The mortality rate is high in individuals more than 60 years of age, of about 16%. [95]  

Prolonged untreated or undertreated hyperthyroidism is associated with an increased risk of acute cardiovascular events, atrial fibrillation, ischemic stroke, osteoporosis, infertility, abnormalities of menstrual cycles, and mortality. [96] [97] [98] [99]  Subclinical hyperthyroidism has been associated with an increased risk of arrhythmias such as atrial fibrillation, osteoporosis, hip fractures, and mortality. [100] [2] [101]

  • 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 on the signs and symptoms of extreme hyperthyroidism (thyroid storm).

  • Pearls and Other Issues

Acute coronary syndrome (ACS) may be complicated by 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%. [102]

Pregnancy and concurrent thyroid pathology can pose 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. The 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. [103]  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 two variants of neonatal thyrotoxicosis: autoimmune-mediated and non-autoimmune-mediated. Autoimmune fetal hyperthyroidism involves the transplacental passage of TSH receptor-stimulating antibodies. Hyperthyroidism is usually 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). Unlike the autoimmune etiology, the non-autoimmune variant is permanent, long persisting after birth. [104]

  • 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.

Primary care clinicians 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. Still, thyroid storm strongly warrants consultation with an endocrinologist and possible admission to the intensive care unit due to potentially life-threatening complications such as tachycardia and hypertensive crisis. Therefore, nurses and physician assistants involved with patient care should be vigilant about the signs and symptoms of thyroid storm.

As mentioned, 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. Therefore, incorporating a mandatory pregnancy test into 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 must review prescriptions, check for drug interactions, and educate patients.

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

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Algorithm for evaluation of patients presenting with hyperthyroidism Contributed by Jasleen Kaur, MD. Created using BioRender.

Disclosure: Philip Mathew declares no relevant financial relationships with ineligible companies.

Disclosure: Jasleen Kaur declares no relevant financial relationships with ineligible companies.

Disclosure: Prashanth Rawla declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

  • Cite this Page Mathew P, Kaur J, Rawla P. Hyperthyroidism. [Updated 2023 Mar 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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  • The clinical evaluation of patients with subclinical hyperthyroidism and free triiodothyronine (free T3) toxicosis. [Am J Med. 1994] The clinical evaluation of patients with subclinical hyperthyroidism and free triiodothyronine (free T3) toxicosis. Figge J, Leinung M, Goodman AD, Izquierdo R, Mydosh T, Gates S, Line B, Lee DW. Am J Med. 1994 Mar; 96(3):229-34.
  • Hyperthyroidism (Nursing). [StatPearls. 2024] Hyperthyroidism (Nursing). Mathew P, Kaur J, Rawla P, Fortes K. StatPearls. 2024 Jan
  • Review A clinical and therapeutic approach to thyrotoxicosis with thyroid-stimulating hormone suppression only. [Am J Med. 2005] Review A clinical and therapeutic approach to thyrotoxicosis with thyroid-stimulating hormone suppression only. Papi G, Pearce EN, Braverman LE, Betterle C, Roti E. Am J Med. 2005 Apr; 118(4):349-61.
  • [Autonomy of the thyroid gland: is there an "organ hyperthyroidism" of "euthyroid" patients?]. [Med Klin (Munich). 2000] [Autonomy of the thyroid gland: is there an "organ hyperthyroidism" of "euthyroid" patients?]. Wawrzyn H, Hesch RD. Med Klin (Munich). 2000 Aug 15; 95(8):421-8.
  • Review Evaluation of thyroid status in patients with thyrotoxicosis. [Clin Chem. 1996] Review Evaluation of thyroid status in patients with thyrotoxicosis. Braverman LE. Clin Chem. 1996 Jan; 42(1):174-8.

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8 Hyperthyroidism Nursing Care Plans

hyperthyroidism case study nursing

Use this nursing care plan and management guide to provide care for patients with hyperthyroidism. Enhance your understanding of nursing assessment , interventions, goals, and nursing diagnosis , all specifically tailored to address the unique needs of individuals with hyperthyroidism.

Table of Contents

What is hyperthyroidism, nursing problem priorities, nursing assessment, nursing diagnosis, nursing goals, 1. managing cardiac symptoms, 2. preventing fatigue and enhancing energy balance, 3. maintaining adequate nutrition balance, 4. reducing anxiety and providing emotional support, 5. maintaining tissue integrity, 6. improving thought processes, 7. initiating patient education and health teachings, 8. administer medications and provide pharmacologic support, 9. monitoring results of diagnostic and laboratory procedures, recommended resources.

Hyperthyroidism , also known as Grave’s disease, Basedow’s disease , or thyrotoxicosis  is a metabolic imbalance that results from the overproduction of thyroid hormones triiodothyronine (T3) and thyroxine (T4). The most common form is Graves’ disease, but other forms of hyperthyroidism include toxic adenoma, TSH-secreting pituitary tumor , subacute or silent thyroiditis, and some forms of thyroid cancer .

A thyroid storm  is a rarely encountered manifestation of hyperthyroidism that can be precipitated by such events as thyroid ablation (surgical or radioiodine), medication overdosage, and trauma . This condition constitutes a medical emergency.

Nursing Care Plans and Management

The nursing care plan and management for patients with hyperthyroidism are focused on promoting optimal thyroid hormone balance, symptom management, and patient education . These goals include ensuring adherence to medication regimen, monitoring vital signs, and assessing for signs of thyroid storm.

The following are the nursing priorities for patients with hyperthyroidism:

  • Monitor thyroid function and hormone levels regularly.
  • Administer appropriate medications, such as antithyroid drugs or beta blockers.
  • Monitor and manage symptoms associated with hyperthyroidism, such as rapid heart rate or weight loss.

Assess for the following subjective and objective data:

  • Rapid heartbeat (tachycardia)
  • Increased appetite and unintentional weight loss
  • Excessive sweating and heat intolerance
  • Nervousness, irritability, and anxiety
  • Tremors or shaking of the hands
  • Fatigue or muscle weakness
  • Difficulty sleeping ( insomnia )
  • Changes in menstrual patterns
  • Frequent bowel movements or diarrhea
  • Enlarged thyroid gland (goiter)
  • Fine, brittle hair and thinning of the skin
  • Bulging eyes (exophthalmos) in Graves’ disease, a specific form of hyperthyroidism.

Following a thorough assessment, a nursing diagnosis is formulated to specifically address the challenges associated with hyperthyroidism based on the nurse ’s clinical judgement and understanding of the patient’s unique health condition. While nursing diagnoses serve as a framework for organizing care, their usefulness may vary in different clinical situations. In real-life clinical settings, it is important to note that the use of specific nursing diagnostic labels may not be as prominent or commonly utilized as other components of the care plan. It is ultimately the nurse’s clinical expertise and judgment that shape the care plan to meet the unique needs of each patient, prioritizing their health concerns and priorities.

Goals and expected outcomes may include:

  • The client will maintain adequate cardiac output for tissue needs as evidenced by stable vital signs, palpable peripheral pulses, good capillary refill, usual mentation, and absence of dysrhythmias.
  • The client will verbalize an increase in the level of energy.
  • The client will display an improved ability to participate in desired activities.
  • The client will maintain the usual reality orientation.
  • The client will recognize changes in thinking/behavior and causative factors.
  • The client will demonstrate stable weight with  normal laboratory values  and be free of signs of malnutrition.
  • The client will report reduced anxiety to a manageable level.
  • The client will maintain moist eye membranes, free of ulcerations.
  • The client will identify measures to provide protection for the eyes and prevent complications.
  • The client will verbalize understanding of the disease process, therapeutic needs, and potential complications.
  • The client will identify the relationship of signs/symptoms to the disease process and correlate symptoms with causative factors.
  • The client will initiate necessary lifestyle changes and participate in the treatment regimen.

Nursing Interventions and Actions

Therapeutic interventions and nursing actions for patients with hyperthyroidism may include:

Hyperthyroidism can cause a hypermetabolic state which leads to an increased demand for oxygen and nutrients by the body, including the heart. This increased demand can lead to an increase in cardiac load and a decrease in cardiac output, which can be further exacerbated by alterations in heart rate, rhythm, and conduction, as well as changes in venous return and vascular resistance. If left uncontrolled, these factors can contribute to a higher risk of reduced cardiac output and potentially even heart failure in patients with hyperthyroidism.

Observe signs and symptoms of severe thirst, dry mucous membranes, weak or thready pulse, poor capillary refill, decreased urinary output, and hypotension . Rapid dehydration can occur, which reduces the circulating volume and compromises cardiac output.

Note history of asthma and bronchoconstrictive disease, sinus bradycardia and heart blocks, advanced HF, or current pregnancy. The presence or potential recurrence of these conditions affects the choice of therapy. For example, use of [beta]-adrenergic blocking agents are contraindicated.

Observe for adverse side effects of adrenergic antagonists: severe decrease in pulse, BP; signs of vascular congestion /HF; cardiac arrest. Indicates the need for reduction or discontinuation of therapy.

Investigate reports of chest pain or angina. This may reflect increased myocardial oxygen demands or ischemia .

Assess pulse and heart rate while the patient is sleeping. Provides a more accurate assessment of tachycardia.

Auscultate heart sounds, note extra heart sounds, development of gallops, and systolic murmurs. Prominent S 1 and murmurs are associated with a forceful cardiac output of a hypermetabolic state; the development of S 3 may warn of impending cardiac failure.

Auscultate breath sounds. Note adventitious sounds. An early sign of pulmonary congestion, reflecting developing cardiac failure.

Monitor BP lying, sitting, and standing, if able. Note widened pulse pressure. General or orthostatic hypotension may occur as a result of excessive peripheral vasodilation and decreased circulating volume. Widened pulse pressure reflects a compensatory increase in stroke volume and decreased systemic vascular resistance (SVR).

Monitor temperature; provide a cool environment, limit bed linens or clothes, and administer tepid sponge baths. Fever (may exceed 104°F) may occur as a result of excessive hormone levels and can aggravate diuresis and/or dehydration and cause increased peripheral vasodilation, venous pooling, and hypotension.

Record I&O. Note urine specific gravity. Significant fluid losses through vomiting , diarrhea , diuresis, and diaphoresis can lead to profound dehydration , concentrated urine, and weight loss.

Weigh daily. Encourage chair rest or bed rest . Limit unnecessary activities. Activity increases metabolic and circulatory demands, which may potentiate cardiac failure.

Monitor ECG , noting rate and rhythm. Document dysrhythmias. Tachycardia (greater than normally expected with fever and/or increased circulatory demand) may reflect direct myocardial stimulation by thyroid hormone. Dysrhythmias often occur and may compromise cardiac output.

Monitor central venous pressure (CVP), if available. Provides a more direct measure of circulating volume and cardiac function.

Monitor laboratory and diagnostic studies . See Laboratory and Diagnostic Procedures

Provide supplemental O 2 as indicated. May be necessary to support increased metabolic demands and/or O 2 consumption.

Provide a hypothermia blanket as indicated. Occasionally used to lower uncontrolled hyperthermia (104°F and higher) to reduce metabolic demands/O 2   consumption and cardiac workload.

Administer IV fluids as indicated. Rapid fluid replacement may be necessary to improve circulating volume but must be balanced against signs of cardiac failure and the need for inotropic support.

Administer medications as indicated. See Pharmacologic Management

Administer transfusions; assist with plasmapheresis, hemoperfusion, and dialysis. May be done to achieve rapid depletion of the extrathyroidal hormone pool in a desperately ill or comatose patient.

Prepare for possible surgery . Subtotal thyroidectomy (removal of five-sixths of the gland) may be the treatment of choice for hyperthyroidism once a euthyroid state is achieved.

Fatigue is a common symptom of hyperthyroidism, which can be related to the hypermetabolic state that increases the demand for energy in the body, leading to exhaustion. The hyperactivity of the central nervous system and alterations in body chemistry, including changes in hormone levels and electrolyte imbalances, can contribute to feelings of fatigue and weakness in individuals with hyperthyroidism.

Monitor vital signs, noting pulse rate at rest and when active. Pulse is typically elevated and, even at rest, tachycardia (up to 160 beats/min) may be noted.

Note the development of tachypnea, dyspnea , pallor, and cyanosis . O 2 demand and consumption are increased in the hypermetabolic state, potentiating the risk of hypoxia with activity.

Provide a quiet environment; cool room, decreased sensory stimuli, soothing colors, and quiet music. Reduces stimuli that may aggravate agitation, hyperactivity, and insomnia.

Encourage the patient to restrict activity and rest in bed as much as possible. Helps counteract the effects of increased metabolism.

Provide comfort measures: touch therapy or massage, cool showers. Patients with dyspnea will be most comfortable sitting in a high Fowler’s position. May decrease nervous energy, promoting relaxation.

Provide diversional activities that are calming, e.g., reading, radio, and television. Allows for use of nervous energy in a constructive manner and may reduce anxiety.

Avoid topics that irritate or upset patients. Discuss ways to respond to these feelings. Increased irritability of the CNS may cause the patient to be easily excited, agitated, and prone to emotional outbursts.

Discuss with SO reasons for fatigue and emotional lability. Understanding that the behavior is physically based may enhance coping with the current situation and encourage SO to respond positively and provide support for the patient.

Administer medications as indicated: Sedatives such as phenobarbital (Luminal); antianxiety agents; chlordiazepoxide (Librium) See Pharmacologic Management

Patients with hyperthyroidism often experience weight loss due to increased metabolic rate, decreased appetite, and increased nutrient utilization. The excess production of thyroid hormones speeds up the body’s metabolism, causing a higher rate of calorie burning and subsequent weight loss. Moreover, the increased metabolic activity may lead to increased nutrient requirements and nutrient depletion, necessitating a focus on adequate nutrition and nutrient supplementation to address potential deficiencies.

Monitor daily food intake. Weigh daily and report losses. Continued weight loss in the face of adequate caloric intake may indicate failure of antithyroid therapy.

Encourage the patient to eat and increase the number of meals and snacks. Give or suggest high-calorie foods that are easily digested. Aids in keeping caloric intake high enough to keep up with the rapid expenditure of calories caused by the hypermetabolic state.

Provide a balanced diet, with six meals per day. To promote weight gain. Note: If the patient has edema, suggest a low- sodium diet.

Avoid foods that increase peristalsis and fluids that cause diarrhea . Increased motility of the GI tract may result in diarrhea and impair the absorption of needed nutrients.

Consult with a dietitian to provide a diet high in calories, protein, carbohydrates, and vitamins. May need assistance to ensure adequate intake of nutrients, and identify appropriate supplements.

Administer medications as indicated: glucose , vitamin B complex, and insulin (small doses). Given to meet energy requirements and prevent or correct hypoglycemia . Insulin aids in controlling serum glucose if elevated.

Anxiety is a common symptom of hyperthyroidism, which can be related to the hypermetabolic state that increases the body’s production of stress hormones, such as cortisol, and the pseudo-catecholamine effect of thyroid hormones. This can lead to an overstimulation of the sympathetic nervous system, causing symptoms of anxiety, nervousness, and irritability in individuals with hyperthyroidism.

Observe behavior indicative of the level of anxiety. Mild anxiety may be displayed by irritability and insomnia. Severe anxiety progressing to the panic state may produce feelings of impending doom, terror, inability to speak or move, shouting, or swearing.

Monitor physical responses, noting palpitations, repetitive movements, hyperventilation, and insomnia. Increased number of [beta]-adrenergic receptor sites, coupled with effects of excess thyroid hormones, produce clinical manifestations of catecholamine excess even when normal levels of norepinephrine or epinephrine exist.

Stay with the patient, maintaining a calm manner. Acknowledge fear and allow the patient’s behavior to belong to the patient. Affirms to the patient or SO that although the patient feels out of control, the environment is safe. Avoiding personal responses to inappropriate remarks or actions prevents conflicts or overreactions to a stressful situation.

Describe and explain procedures, the surrounding environment, or sounds that may be heard by the patient. Provides accurate information, which reduces distortions and confusion that can contribute to anxiety and/or fear reactions.

Speak in brief statements. Use simple words. Attention span may be shortened, and concentration reduced, limiting the ability to assimilate information.

Reduce external stimuli: Place in a quiet room; provide soft, soothing music; reduce bright lights; reduce the number of persons having contact with the patient. Creates a therapeutic environment; shows recognition that unit activity or personnel may increase patient’s anxiety.

Discuss with the patient and/or SO reasons for emotional lability and/or psychotic reaction. Understanding that behavior is physically based enhances acceptance of the situation and encourages different responses and approaches.

Reinforce the expectation that emotional control should return as drug therapy progresses. Provides information and reassures the patient that the situation is temporary and will improve with treatment.

Administer antianxiety agents or sedatives and monitor their effects. May be used in conjunction with a medical regimen to reduce the effects of hyperthyroid secretion.

Refer to support systems as needed: counseling, social services, pastoral care. Ongoing therapy support may be desired or required by the patient/SO if the crisis precipitates lifestyle alterations

Due to alterations in the protective mechanisms of the eye, including impaired closure of the eyelid and the development of exophthalmos (protrusion of the eyeball). These changes can lead to an increased risk of eye infections, corneal ulcers, and other complications that can impair tissue integrity and compromise visual function in individuals with hyperthyroidism.

Encourage the use of dark glasses when awake and taping the eyelids shut during sleep as needed. Suggest the use of sunglasses or eyepatch. Moisten conjunctiva often with isotonic eye drops. Protects exposed cornea if the patient is unable to close eyelids completely because of edema or fibrosis of fat pads and/or exophthalmos.

Elevate the head of the bed and restrict salt intake if indicated. Decreases tissue edema when appropriate: HF, which can aggravate existing exophthalmos.

Instruct patient in extraocular muscle exercises if appropriate. Improves circulation and maintains the mobility of the eyelids.

Provide an opportunity for the patient to discuss feelings about altered appearance and measures to enhance self-image. Protruding eyes may be viewed as unattractive. Appearance can be enhanced with the proper use of makeup, overall grooming , and the use of shaded glasses.

Administer medications as indicated . See Pharmacologic Management

Prepare for possible surgery as indicated. Eyelids may need to be sutured shut temporarily to protect the corneas until edema resolves (rare) or increasing space within the sinus cavity and adjusting musculature may return the eye to a more normal position.

Patients with hyperthyroidism may experience changes in their thought processes due to the effects of excess thyroid hormone on the brain and nervous system. These changes can include increased irritability, anxiety, restlessness, difficulty concentrating, and rapid or racing thoughts.

Assess the thinking process. Determine attention span, and orientation to place, person, or time. Determines the extent of interference with sensory processing

Note changes in behavior. May be hypervigilant, restless, extremely sensitive, or crying or may develop frank psychosis.

Assess the level of anxiety. Anxiety may alter thought processes.

Provide a quiet environment; decreased stimuli, cool room, dim lights. Limit procedures and/or personnel. Reduction of external stimuli may decrease hyperactivity or reflexes, CNS irritability, and auditory and/or visual hallucinations.

Reorient to person, place, or time as indicated. Helps establish and maintain awareness of reality and the environment.

Present reality concisely and briefly without challenging illogical thinking. Limits defensive reaction.

Provide a clock, calendar, and room with an outside window; alter the level of lighting to simulate day or night. Promotes continual orientation cues to assist the patient in maintaining a sense of normalcy.

Encourage visits by family and/or SO. Provide support as needed. Aids in maintaining socialization and orientation. Note: The patient’s agitation and/or psychotic behavior may precipitate family conflicts.

Provide safety measures. Pad side rails, close supervision, and applying soft restraints as last resort as necessary. Prevents injury to the patient who may be hallucinating or disoriented.

Administer medication as indicated: sedatives, antianxiety agents, and/or antipsychotic drugs. Promotes relaxation, and reduces CNS hyperactivity and agitation to enhance thinking ability.

Patient education and health teachings for patients with hyperthyroidism include providing information about the condition, its causes, symptoms, and potential complications. Patients should be educated about the importance of medication adherence, regular follow-up appointments, and lifestyle modifications such as stress management, adequate rest, and a balanced diet to support the patient’s well-being and thyroid health.

Identify signs and symptoms requiring medical evaluation : fever, sore throat , and skin eruptions. Early identification of toxic reactions (thiourea therapy) and prompt intervention are important in preventing the development of agranulocytosis.

Monitor CBC periodically. To detect leukopenia, thrombocytopenia, and agranulocytosis if the patient is taking propylthiouracil and methimazole . Instruct to take medications with meals to minimize GI distress and to avoid OTC cough preparations because many contain iodine.

Identify stressors and discuss precipitators to thyroid crises: personal or social and job concerns, infection , pregnancy. Psychogenic factors are often of prime importance in the occurrence and/or exacerbation of this disease.

Review the disease process and future expectations. Provides a knowledge base from which patients can make informed choices.

Provide information appropriate to the individual situation. This information includes the severity of the condition, cause, age, and concurrent complications to determine the course of treatment.

Provide information about the signs and symptoms of hypothyroidism and the need for continuous follow-up care. A patient who has been treated for hyperthyroidism needs to be aware of the possible development of hypothyroidism , which can occur immediately after treatment or as long as 5 yr later.

After Radioactive Iodine (I-131) therapy, tell the patient not to expectorate or cough freely. Stress the need for repeated measurement of serum T4 levels. Saliva will be radioactive for 24 hours.

Discuss drug therapy, including the need for adhering to the regimen, and expected therapeutic and side effects. Antithyroid medication (either as primary therapy or in preparation for thyroidectomy) requires adherence to a medical regimen over an extended period to inhibit hormone production. Agranulocytosis is the most serious side effect that can occur, and alternative drugs may be given if problems arise.

Explain the need to check with a physician and/or pharmacist before taking other prescribed or OTC drugs. Antithyroid medications can affect or be affected by numerous other medications, requiring monitoring of medication levels, side effects, and interactions.

Emphasize the importance of planned rest periods. Prevents undue fatigue; reduces metabolic demands. As the euthyroid state is achieved, stamina and activity levels will increase.

Review the need for a nutritious diet and periodic review of nutrient needs. Tell the patient to avoid caffeine, red/yellow food dyes, and artificial preservatives. Provides adequate nutrients to support the hypermetabolic state. A hormonal imbalance is corrected, and the diet will need to be readjusted to prevent excessive weight gain. Irritants and stimulants should be limited to avoid cumulative systemic effects.

Stress the necessity of continued medical follow-up. Necessary for monitoring the effectiveness of therapy and prevention of potentially fatal complications.

Medications used for the management of hyperthyroidism may include antithyroid drugs such as methimazole or propylthiouracil, which work to reduce the production of thyroid hormones. Beta-blockers like propranolol may be prescribed to alleviate symptoms such as rapid heart rate, tremors, and anxiety. These medications help to regulate thyroid hormone levels and alleviate the associated symptoms and promote thyroid function.

Thyroid hormone antagonists: propylthiouracil (PTU), methimazole (Tapazole) May be a definitive treatment or used to prepare the patient for surgery, but the effect is slow and so may not relieve thyroid storm. Once PTU therapy is begun, abrupt withdrawal may precipitate a thyroid crisis. Acts to prevent the release of thyroid hormone into circulation by increasing the amount of thyroid hormone stored within the gland. May interfere with RAI treatment and may exacerbate the disease in some people.

Beta-blockers: propranolol (Inderal), atenolol (Tenormin), nadolol (Corgard), pindolol (Visken) Given to control the thyrotoxic effects of tachycardia, tremors, and nervousness, and is the first drug of choice for an acute storm. Decreases heart rate or cardiac work by blocking [beta]-adrenergic receptor sites and blocking the conversion of T4 to T3. If severe bradycardia develops, atropine may be required. Blocks thyroid hormone synthesis and inhibits the peripheral conversion of T4 to T3.

Strong iodine solution (Lugol’s solution) or supersaturated potassium iodide (SSKI) PO May be used as surgical preparation to decrease the size and vascularity of the gland or to treat thyroid storm. Should be started 1–3 hr after initiation of antithyroid drug therapy to minimize hormone formation from the iodine. If iodide is part of the treatment, mix it with milk juice, or water to prevent GI distress and administer it through a straw to prevent tooth discoloration.

RAI (Na131I or Na125I) following NRC regulations for radiopharmaceutical Radioactive iodine therapy is the treatment of choice for almost all patients with Graves’ disease because it destroys abnormally functioning gland tissue. Peak results take 6–12 wk (several treatments may be necessary); however, a single dose controls hyperthyroidism in about 90% of patients. This therapy is contraindicated during pregnancy. Also, people preparing or administering the dose must have their own thyroid burden measured, and contaminated supplies and equipment must be monitored and stored until decayed.

Corticosteroids: dexamethasone (Decadron) Provides glucocorticoid support. Decreases hyperthermia; relieves relative adrenal insufficiency; inhibits calcium absorption; and reduces the peripheral conversion of T3 from T4. May be given before thyroidectomy and discontinued after surgery.

Digoxin (Lanoxin) Digitalization may be required in patients with HF before [beta]-adrenergic blocking therapy can be considered or safely initiated.

Potassium (KCl, K-Lyte) Increased losses of K+ through intestinal and/or renal routes may result in dysrhythmias if not corrected.

Acetaminophen (Tylenol) Drug of choice to reduce temperature and associated metabolic demands. Aspirin is contraindicated because it actually increases the level of circulating thyroid hormones by blocking the binding of T3 and T4 with thyroid-binding proteins.

Sedative, barbiturates Promotes rest, thereby reducing metabolic demands and cardiac workload.

Furosemide ( Lasix ) Diuresis may be necessary if HF occurs. It also may be effective in reducing calcium level if the neuromuscular function is impaired.

Muscle relaxants Reduces shivering associated with hyperthermia, which can further increase metabolic demands.

Sedatives such as phenobarbital (Luminal); antianxiety agents; chlordiazepoxide (Librium) Combats nervousness, hyperactivity, and insomnia.

Methylcellulose drops Lubricates the eyes, reducing the risk of lesion formation.

Adrenocorticotropic hormone (ACTH), prednisone Given to decrease rapidly progressive and marked inflammation.

Antithyroid drugs May decrease signs and symptoms or prevent the worsening of the condition.

Laboratory and diagnostic procedures for patients with hyperthyroidism commonly include thyroid function tests such as measurement of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and total or free triiodothyronine (T3). These tests help evaluate the levels of thyroid hormones in the blood and determine the functioning of the thyroid gland. While potassium and calcium tests are done to assess the electrolyte balance and detect any abnormalities that may occur due to the thyroid hormone imbalance.

Serum potassium Hypokalemia resulting from intestinal losses, altered intake, or diuretic therapy may cause dysrhythmias and compromise cardiac function/output. In the presence of thyrotoxic paralysis (primarily occurring in Asian men), close monitoring and cautious replacement are indicated because rebound hyperkalemia can occur as the condition abates releasing potassium from the cells.

Serum calcium Elevation may alter cardiac contractility.

Sputum culture Pulmonary infection is the most frequent precipitating factor of crisis.

Serial ECGs May demonstrate the effects of electrolyte imbalance or ischemic changes reflecting inadequate myocardial oxygen supply in the presence of increased metabolic demands.

Chest X-ray s Cardiac enlargement may occur in response to increased circulatory demands. Pulmonary congestion may be noted with cardiac decompensation.

Recommended nursing diagnosis and nursing care plan books and resources.

Disclosure: Included below are affiliate links from Amazon at no additional cost from you. We may earn a small commission from your purchase. For more information, check out our privacy policy .

Ackley and Ladwig’s Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care We love this book because of its evidence-based approach to nursing interventions. This care plan handbook uses an easy, three-step system to guide you through client assessment, nursing diagnosis, and care planning. Includes step-by-step instructions showing how to implement care and evaluate outcomes, and help you build skills in diagnostic reasoning and critical thinking.

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All-in-One Nursing Care Planning Resource – E-Book: Medical-Surgical, Pediatric, Maternity, and Psychiatric-Mental Health   Includes over 100 care plans for medical-surgical, maternity/OB, pediatrics, and psychiatric and mental health. Interprofessional “patient problems” focus familiarizes you with how to speak to patients.

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5 thoughts on “8 Hyperthyroidism Nursing Care Plans”

Super post. Do you have any other ones you can give? I like super stuff. :)

This content has really improved my knowledge about hyperthyroidism. Thank you so much

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Hi Arom, Awesome to know the hyperthyroidism care plans are making your nursing life easier! If you need more tips or info on anything else, feel free to reach out. Here to help!

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  • History of Present Illness
  • Review of Systems

Past Medical History

  • Physical Examination
  • Differential Diagnosis
  • Initial Studies
  • Lab Results
  • Differential Diagnosis 2
  • Relevant Testing
  • Test Results
  • Imaging Results
  • Test Interpretation
  • Treatment Orders
  • About the Case

31-year-old woman with nausea and increased thirst

hyperthyroidism case study nursing

  • Medical history : Primary hyperthyroidism due to Graves disease treated with radioactive iodine 6 years prior with subsequent hypothyroidism; depression 5 years prior that resolved with medication and counseling; no other psychiatric disorder. No known diabetes, pulmonary, or renal disease.
  • Surgical history : None
  • Medications : Levothyroxine 125 mcg daily, vitamin D 800 U daily.
  • Allergies : No known drug allergies.
  • Family history : Mother has type 2 diabetes mellitus and primary hypothyroidism.
  • Social history : Patient is married and has been a homemaker since the birth of her daughter 2 years ago. She used to work in an office. She is a nonsmoker, has no alcohol intake, and denies taking any recreational drugs. Her diet is healthy and balanced. She eats a moderate amount of dairy products, lean meat, fruit, and vegetables. She last traveled abroad 6 months ago to Portugal. She has not had any recent contact with anyone with febrile illness or GI symptoms.

Hyperthyroidism Case Study (75 min)

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Mrs. Black is a 31 year old female who is 2 weeks postpartum.  This morning her husband found her difficult to rouse and confused, and called 911.  The husband indicates she has been quite anxious since the birth of their first child. He reports she has had nausea and vomiting for two days, as well as watery diarrhea and generalized abdominal pain.  She hasn’t been able to breastfeed baby because she’s been too anxious. Husband denies any sick contacts or recent travel.

What other medical history would you want to attempt to gather from the husband?

  • Any complications with the pregnancy or delivery?
  • Characteristics of vomit/diarrhea? Any bleeding?
  • Medical conditions
  • Medications taken on a daily basis

What initial nursing assessments should be performed?

  • Neuro assessment – Level of consciousness, pupils, strength/movements
  • Abdominal assessment due to diarrhea and vomiting, assess for any masses, tenderness, or guarding with palpation
  • Full set of vital signs
  • Skin assessment – color, temperature, condition
  • Heat and lung sounds and respiratory/airway status

Upon further questioning, the husband reports Mrs. Black has a history of Hyperlipidemia, Graves Disease, and asthma and takes simvastatin and propylthiouracil daily, plus her rescue inhaler when she needs it. Upon assessment, Mrs. Black is somnolent and only minimally responsive to painful stimuli. She is unable to answer orientation questions and just keeps repeating her husband’s name.  The nurse notes redness to her eyes and swelling around her eyelids. Heart rate is rapid and irregular. Lungs have diffuse crackles bilaterally. Vital signs are as follows:

BP 120/76 mmHg

Temp 101°F 

SpO 2 89% on 4L nasal cannula

What should the nurse’s first action be?

Based on the information you have, what diagnostic laboratory tests would you anticipate the provider ordering.

  • Full metabolic panel for electrolytes, renal function, etc.
  • Thyroid panel
  • Complete blood count to assess for infection or occult bleeding
  • Arterial Blood Gas to assess oxygenation / ventilation / gas exchange

Mrs. Black becomes more obtunded and her heart rate goes up to 155. The provider orders a 12-lead EKG and proceeds to prepare for intubation for airway protection. The Respiratory Therapist comes to bedside and notes the patient has a swollen thyroid gland. For this reason, the Anesthesia team is called to the bedside to assist in a successful intubation. The provider orders a full lab panel, including CBC, CMP, LFTs, and a Thyroid Panel, plus an Arterial Blood Gas, and consults the ICU team to admit Mrs. Black.

This is the 12-lead EKG:

12 Lead EKG

By James Heilman, MD – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=19126125

Interpret this EKG. What are the implications of this rhythm for the patient?

  • Atrial Fibrillation with Rapid Ventricular Response (rapid rate, >150)
  • This severe tachycardia with arrhythmia can be detrimental to the patient’s cardiac output, especially if this is not her baseline
  • It may also indicate underlying electrolyte abnormalities and/or other hormonal changes that are causing the severe tachycardia
  • No one’s heart can tolerate this fast blood pressure for that long
  • Mrs. Black likely has a large goiter, this could cause obstruction of the airway and create for a difficult intubation.
  • The Anesthesia team is considered the expert consultants for airways within the hospital, most times. They are not only experts, but they can also bring equipment with them to assist with more difficult airways

Lab results return on Mrs. Black as she is transferred to the ICU:

Na 144 pH 7.33 TSH 0.1

K 5.0 pCO 2 48 WBC 14K

Mg 1.0 HCO 3 – 24 Hgb 12.5

BUN 11 pO 2 190 Hct 38%

Cr 0.7 Lactate 3.2 Plt 450K

What is going on physiologically with Mrs. Black?

  • Mrs. Black is likely experiencing a Thyroid Storm or Thyroid Crisis. This causes severe tachycardia and arrhythmias, N/V/D, and a severe febrile state.
  • Remember hyperthyroidism is ‘hypermetabolic’ – so now those things have become severe
  • The low TSH level is the clue that her thyroid hormone levels are likely sky high, you can count on that, even without the actual Thyroxine levels.

What medications do you anticipate the provider ordering for Mrs. Black?

  • Beta blocker or calcium channel blocker to address the hypertension and tachycardia
  • Propylthiouracil or methimazole as antithyroid therapy
  • Any other medications required to address the symptoms during the crisis (antipyretics, antidiarrheals, antiemetics, etc.)

The provider orders a beta blocker and IV fluids for Mrs. Black, as well as an increased dose of propylthiouracil (PTU).  She is stable for now, but it may take a few days for her to overcome this thyroid storm/crisis. Her husband asks the nurse what caused this.

What is the best response to the husband to explain what triggered Mrs. Black’s Thyroid Storm/Crisis?

  • The stress of the pregnancy and delivery are likely the initial trigger.
  • The start of the Thyroid Crisis will have caused some anxiety for her and then continued to be further exacerbated due to excess stress

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Patient W arrived for her regular yearly physical exam. She is 60 years of age and has always been healthy and active. Patient W caught the attention of Nurse S because she was wearing a turtleneck sweater, slacks, and a light jacket, even though it was a sunny and warm day. When Nurse S asked how the patient was feeling, the answer was, "I've been trying hard to diet, but I still gained 12 pounds this past year. Maybe it's that I'm not exercising as much since my arthritis has kicked up. I've been having a lot of pain and stiffness in my joints." Further questioning revealed that Patient W had also developed chronic constipation. The physician examined the patient and ordered laboratory work to be done prior to her next visit, scheduled for two weeks. When the laboratory work returned, it showed an elevated TSH and a decrease in both T 3 and T 4 levels. Patient W was prescribed a starting dose of levothyroxine at 25 mcg daily. Nurse S spent time teaching the patient about taking the tablet at the same time each day with a full glass of water. Because she was not taking any other medications, there should be no problem with drug interactions; however, the patient was instructed not to take an antacid within four hours of taking the medication in order to avoid problems with malabsorption. A follow-up appointment was scheduled for four weeks with instructions to repeat the blood work one week prior to that appointment. At that time, medication dosages would be adjusted.

The next weekend, Nurse S went to her family reunion, where she was cornered by her cousin, Patient A, asking her advice. The cousin had noticed a hard, painless nodule near his Adam's apple. He was clearly concerned, due in part to the fact that he remembered the course of treatment his father had gone through 30 years prior for thyroid cancer. Nurse S had her cousin tilt his head back, then looked at his throat area while he swallowed some iced tea. She clearly saw a lump protruding prominently from the neck area. She advised him to call his physician for an appointment as soon as possible to be checked out. She told him to expect to have blood work drawn and an ultrasound of the thyroid.

Patient A followed Nurse S's advice and called her two weeks after he had seen the doctor and had the diagnostic work done. The ultrasound had showed nodules, so a biopsy was arranged. When it returned from the pathologist, the biopsy was positive for papillary adenocarcinoma. A total thyroidectomy was done, and Patient A had an uneventful recovery. Pathology showed no metastasis to lymph glands, so he did not have to face a difficult course of treatment like his father had.

The next week at work in the office, there was a problem with the air conditioning unit. The temperature was uncomfortably cold for most patients. However, Patient C, who had come to the office for a work-related physical exam, complained of being hot. She was wearing a sleeveless blouse and was fanning herself despite the cool room. At 27 years of age, Nurse S felt it was unlikely that Patient C was suffering from menopause, so she mentioned the symptom in her notes for the physician. The patient's measured weight was 116 pounds, which she reported was a loss of 12 pounds. She had not been dieting and reported feeling nervous and restless lately, which she attributed to a recent miscarriage.

When the nurse reported these findings to the physician, he ordered TSH, T 3 , and T 4 levels to be drawn. At the follow-up appointment, results from the blood studies showed a decrease in TSH and an increase in both the T 3 and T 4 . All indications were for a diagnosis of hyperthyroidism.

The patient was prescribed methimazole, the thyroid-suppressing medication. In addition, the physician indicated that if there was no improvement in one month, he would order a thyroid scan. Fortunately, like most patients, Patient C responded positively to treatment with the methimazole, and one year later she returned for follow-up with her baby boy.

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nursing diagnosis for hyperthyroidism

Hyperthyroidism Nursing Diagnosis and Nursing Care Plan

Last updated on May 18th, 2022 at 08:53 am

Hyperthyroidism Nursing Care Plans Diagnosis and Interventions

Hyperthyroidism NCLEX Review and Nursing Care Plans

The thyroid gland is the butterfly-shaped gland at the bottom of the neck, above the collarbone that produces hormone thyroxine.

Hyperthyroidism, also known as hyperactive thyroid, occurs when the thyroid gland secretes too much thyroxine. Hyperthyroidism can cause unexpected weight loss and a quick or irregular heartbeat by speeding up the body’s metabolism.

Hyperthyroidism can be treated in a variety of ways depending on the clinical judgment of the healthcare provider. Anti-thyroid medicines and radioactive iodine are used to reduce thyroid hormone production.

Surgery to remove all or part of the thyroid gland is sometimes used to treat hyperthyroidism. Although untreated hyperthyroidism can be dangerous, most people do well if it is diagnosed and treated.

Signs and Symptoms of Hyperthyroidism

Hyperthyroidism can be similar to other healthcare problems, making it harder to be diagnosed. It can also result in a wide range of signs and symptoms, such as:

  • Weight loss that is unintentional even when the appetite and food intake has increased.
  • Rapid Heartbeat that is usually more than 100 beats per minute
  • Palpitations or pounding of the heart
  • Anxiety , Irritability, and Nervousness
  • A fine trembling usually in the hands and fingers
  • Irregular menstrual patterns
  • Increased heat sensitivity
  • More frequent bowel movements
  • Goiter or an enlarged thyroid gland that may appear at the base of the neck
  • Muscle Weakness
  • Thinning of the skin
  • Fine, brittle hair

It is more common in older adults to exhibit subtle symptoms such as a faster heart rate, sensitivity to warm temperatures, and a tendency to become more tired after performing daily activities. Hyperthyroidism symptoms might be masked by certain medications.

It’s difficult to tell if a patient has hyperthyroidism if they are taking beta-blockers for high blood pressure or another illness.

  • Thyroid eye disease –  happens when the tissues and muscles behind the eyes enlarge and the eyeballs protrude beyond their typical protective orbits.

The following are signs and symptoms of Thyroid Eye Disease:

  • Bulging of the eyes
  • A gritty sensation, discomfort, or pressure in the eyes
  • Inflammation or redness in or around the eyes
  • Puffed-up or pulled-back eyelids
  • Sensitivity to light
  • Loss of vision or double vision

Causes of Hyperthyroidism

Hyperthyroidism can be caused by a number of conditions, including Graves’ disease, Plummer’s disease, and thyroiditis. Too much thyroxine can be caused by a variety of factors, the thyroid normally generates the appropriate quantity of hormones, but it can occasionally create too much T4. This could happen for a variety of reasons, including:

1. Grave’s Disease . It is a chronic illness that affects people of all ages. Graves’ disease is an autoimmune illness in which the immune system’s antibodies cause the thyroid to produce excessive amounts of T4. Hyperthyroidism is most commonly caused by this condition.

2. Thyroid nodules. This can be toxic adenoma, toxic multinodular goiter, or Plummer’s disease. It is when one or more thyroid adenomas produce too much T4, this type of hyperthyroidism develops. An adenoma is a portion of the thyroid gland that has walled itself off from the rest of the gland, resulting in noncancerous (benign) lumps that can cause thyroid enlargement.

3. Thyroiditis. This is an infection or an immune system disorder can cause the thyroid to swell and leak hormones into the bloodstream. In this condition, the thyroid is swollen for no apparent reason. This is often followed by hypothyroidism, in which the thyroid does not make enough hormones. These conditions are usually temporary. Thyroiditis can happen:

  • Following a pregnancy
  • When there is a virus or another immune system problem
  • Too much thyroid medicine is used
  • Too much Iodine in the diet like in medication or supplement

Risk Factors for Hyperthyroidism

Risk factors for hyperthyroidism include:

  • A family history of Hyperthyroidism
  • Female gender
  • Type 1 diabetes , pernicious anemia, primary adrenal insufficiency, or history of chronic diseases.

Diagnosis for Hyperthyroidism

The following tests are used to determine if there is hyperthyroidism:

1. Medical History and Physical Assessment- the healthcare provider may look for a tiny tremor in the fingers when they’re stretched, overactive reflexes, eye changes, and warm, wet skin during the exam. The healthcare provider will also inspect the thyroid gland when swallowing to see whether it is swollen, lumpy, or sensitive, as well as check the pulse for quick or irregular beats.

2. Blood Tests – Thyroid-stimulating hormone (TSH) and thyroxine blood tests can be used to confirm the diagnosis. An overactive thyroid is indicated by high thyroxine levels and low or nonexistent TSH values. Because TSH is the hormone that tells the thyroid gland to generate more thyroxine, the amount of TSH is crucial. These tests are especially important for older adults who may not have classic hyperthyroidism symptoms.

  • Normal TSH level: 0.4 to 4.0 mIU/L
  • Normal T3 level: 100 to 200 ng/dL
  • Normal T4 level: 5.0 to 12.0 μg/dL
  • Normal Free T4 level: 0.8 to 1.8 ng/dL.

If blood tests reveal hyperthyroidism, it is advised to undergo one of the tests below to identify why the thyroid is overactive:

3. Radioiodine uptake test – For this test, a modest amount of radioactive iodine (radioiodine) will be orally ingested to see how much collects in the thyroid gland. To discover how much iodine the thyroid has absorbed, an assessment will be performed after four, six, or 24 hours — and sometimes all three.

A high radioiodine uptake implies that the thyroid gland is overproducing thyroxine. Graves’ illness or hyperfunctioning thyroid nodules are the most likely causes. If hyperthyroidism is present and the patient has a low radioiodine absorption, it means that the thyroxine stored in the thyroid gland is leaking into the bloodstream.

4. Thyroid scan – A radioactive isotope will be injected into a vein on the inside of the elbow or, in some cases, in the vein of the hand. After that, the patient will lie down on a table with the head stretched backward while a unique camera displays an image of the thyroid gland on a computer screen. This test demonstrates how iodine accumulates in the thyroid.

5. Thyroid ultrasound – The thyroid is imaged using high-frequency sound waves in this test. Ultrasound may be more effective than other tests at detecting thyroid nodules, and there is no radiation involved.

Treatment for Hyperthyroidism

Hyperthyroidism can be treated in a variety of ways. The optimal treatment depends on the patient’s age, physical condition, underlying cause, personal preference, and the severity of the disorder. Treatment options include:

1. Radioactive iodine – it is taken by mouth and absorbed by the thyroid gland, causing it to shrink. Symptoms normally go away after a few months. Excess radioactive iodine is excreted from the body in weeks to months.

2. Anti-thyroid medications – These drugs work by preventing the thyroid gland from generating too many hormones and thereby reducing hyperthyroidism symptoms. Symptoms usually improve within a few weeks to months, although anti-thyroid medication treatment often lasts at least a year or longer.

3. Beta-blockers – these are types of medications that are often used to treat high blood pressure and have no effect on thyroid levels, However, they can help with hyperthyroidism symptoms like tremors, rapid heart rate, and palpitations.

4. Surgical procedures (thyroidectomy) – Thyroid surgery may be an option if the patient is pregnant or otherwise unable to tolerate anti-thyroid medications or radioactive iodine therapy. In a thyroidectomy, the surgeon removes the majority of the thyroid gland. The vocal cords and parathyroid glands, damage to the vocal cords and parathyroid glands are at risk from this procedure.

Lifestyle Modification

1. Low-iodine Diet – Once treatment for Hyperthyroidism has begun, the symptoms should start to subside. However, it is recommended to manage Hyperthyroidism with a healthy diet avoid the following:

  • high amounts of poultry or beef
  • dairy products
  • high amounts of grain products (such as bread, pasta, and pastries)
  • iodized salt

2. Exercise- Exercise in general will boost the mood and improve muscle tone, as well as the cardiovascular system. Graves’ disease patients should engage in weight-bearing exercise to help maintain bone density. Exercising can also help reduce appetite and regain energy.

3. Relaxation Techniques – Many relaxation techniques, especially when dealing with illness, can help retain a positive outlook. Stress is known to be a risk factor in Graves’ disease, so learning to relax and create balance will help to preserve physical and emotional health.

Nursing Diagnosis for Hyperthyroidism

Hyperthyroidism nursing care plan 1.

Risk for Decreased Cardiac Output

Nursing Diagnosis: Risk for Decreased Cardiac Output related to increased cardiac workload, changes in venous return and systemic vascular resistance and alterations in rate, rhythm, conduction, secondary to hyperthyroidism.

Desired Outcome: The patient will be able to maintain an adequate cardiac output, as evidenced by stable vital signs, normal capillary refill, palpable peripheral pulses, good mentation, and absence of dysrhythmias.

Hyperthyroidism Nursing Care Plan 2

Nursing Diagnosis: Fatigue related to hypermetabolic state with increased energy requirements and irritability of central nervous system with altered body chemistry, secondary to hyperthyroidism, as evidenced by reduced performance due to an excessive lack of energy to keep up with the daily routine, nervousness, tension, and irritability, and impaired ability to concentrate.

Desired Outcomes:

  • The patient will be able to verbalize increased energy level
  • The patient will show improved participation in desired activities.

Hyperthyroidism Nursing Care Plan 3

Nursing Diagnosis: Anxiety related to central nervous system overstimulation secondary to hyperthyroidism, as evidenced by increased feelings of apprehension, loss of control, panic, changes in cognition, extraneous movements, tremor, and restlessness.

  • The patient will verbalize feeling more relaxed.
  • The patient will report decreased anxiety to a manageable level.
  • The patient will be able to identify healthy coping mechanisms for dealing with emotions.

Hyperthyroidism Nursing Care Plan 4

Risk for Imbalanced Nutrition: Less Than Body Requirements

Nursing Diagnosis: Risk for Imbalanced Nutrition: Less Than Body Requirements related to metabolic imbalance secondary to hyperthyroidism as evidenced by weight loss, nausea , vomiting, diarrhea , and hyperglycemia .

Desired Outcome: The patient will be free for signs of malnutrition as evidenced by stable weight gain, increased appetite, and normal laboratory values.

Hyperthyroidism Nursing Care Plan 5

Deficient Knowledge

Nursing Diagnosis: Deficient Knowledge related to lack of awareness or recall, misinterpretation of the given information, and unawareness of available information sources secondary to hyperthyroidism, as evidenced by questions and requests for additional information, assertions of misunderstanding, and development of avoidable complications.

  • The patient will verbally express understanding of the disease process and possible complications.
  • The patient will be able to link indications and symptoms to the disease process and correlate symptoms to causative factors.
  • The patient will express knowledge of the therapeutic needs.
  • The patient will make the necessary lifestyle modifications and follow the treatment plan.

Nursing References

Ackley, B. J., Ladwig, G. B., Makic, M. B., Martinez-Kratz, M. R., & Zanotti, M. (2020).  Nursing diagnoses handbook: An evidence-based guide to planning care . St. Louis, MO: Elsevier.  Buy on Amazon

Gulanick, M., & Myers, J. L. (2022).  Nursing care plans: Diagnoses, interventions, & outcomes . St. Louis, MO: Elsevier. Buy on Amazon

Ignatavicius, D. D., Workman, M. L., Rebar, C. R., & Heimgartner, N. M. (2018).  Medical-surgical nursing: Concepts for interprofessional collaborative care . St. Louis, MO: Elsevier.  Buy on Amazon

Silvestri, L. A. (2020).  Saunders comprehensive review for the NCLEX-RN examination . St. Louis, MO: Elsevier.  Buy on Amazon


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