Search databaseBooksAll DatabasesAssemblyBiocollectionsBioProjectBioSampleBioSystemsBooksClinVarConserved DomainsdbGaPdbVarGeneGenomeGEO DataSetsGEO ProfilesGTRHomoloGeneIdentical Protein web CatalogNucleotideOMIMPMCPopSetProteinProtein ClustersProtein family ModelsPubChem BioAssayPubChem CompoundPubChem SubstancePubMedSNPSRAStructureTaxonomyToolKitToolKitAllToolKitBookgh Bookshelf. A organization of the national Library of Medicine, nationwide Institutes of Health.

You are watching: A nurse is assessing a client with hyperthyroidism. what findings should the nurse expect?

StatPearls . Sweetheart Island (FL): StatPearls Publishing; 2021 Jan-.



The thyroid gland is a bilobed framework located in the anterior aspect of the trachea in between the cricoid cartilage and also the suprasternal notch. Each lobe of the thyroid connects via a thyroid isthmus. That is provided via the premium 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 created of spherical, polarized follicular cells the surround a gel-like thyroglobulin-rich colloid. Thyroglobulin is the essential precursor because that thyroid hormones and requires iodide to type thyroid hormone. Diet iodine is transported right into thyroid follicular cell via the sodium-iodide symporter after conversion come iodide via thyroid peroxidase enzyme. The process of iodide ending up being incorporated into monoiodotyrosine (MIT) or diiodotyrosine (DIT) molecule is referred to as organification, and also the procedure is reasonably self-regulated. Short dietary iodide promoted upregulation that the sodium-iodide symporter if high dietary iodide in the interim inhibits the organification process, a phenomenon recognized as the Wolff-Chaikoff effect.<1> Iodide incorporation right into the thyroid hormone precursors, MIT and also DIT, is due to the peroxidase enzyme. The necessary coupling the one molecule of MIT v one molecule the DIT leader to the manufacturing of triiodothyronine (T3), while the coupling that 2 DIT molecules leader to thyroxine (T4).

The thyroid gland secretes thyroxine (T4) in solution to thyroid-stimulating hormone (TSH) originating from the anterior pituitary gland. The secreted T4 is convert to a an ext potent and also triiodothyronine (T3) via deiodinase enzymes. Many of the counter of T4 come T3 bring away place exterior the thyroid, return the thyroid gland possesses the intrinsic capacity 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 disclosure anterior pituitary secretion of thyroid-stimulating hormone (TSH), which, in turn, promotes T4 cheap from the thyroid gland. T4 and also T3 exert an adverse feedback control on both the hypothalamus and also the anterior pituitary.

The hatchet "hyperthyroidism" specifies a syndrome linked with overabundance thyroid hormone production. The is a common misconception that the state thyrotoxicosis and also hyperthyroidism space synonyms of one another. The term "thyrotoxicosis" describes a state of excess thyroid hormone exposure come tissues.  return hyperthyroidism can lead to thyrotoxicosis and also can be offered interchangeably, it is crucial to note the difference between them.


In the unified States and most western countries, Graves an illness is the most common cause of hyperthyroidism. As Graves condition is autoimmune in etiology, this form of hyperthyroidism often tends to manifest itself in younger populations. In the enlarge demographic, toxic multinodular goiter is the most common reason of hyperthyroidism.

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

Factitious thyroiditis is hyperthyroidism the is connected with unreasonable or extreme use of pharmaceutical thyroid hormone. Due to a well-received side effect of weight loss, thyroxine has actually the potential for abuse, and any background of a hyperthyroid patient should encompass a medication list and also an evaluate of feasible misuse (whether knowingly or unintentional).

Other sources of hyperthyroidism encompass ectopic foci that thyroxine-secreting tissue. The more prevalent (although rare) kind of this etiology is struma ovarii, consist of of ectopic and functional thyroid organization (often compromising higher than 50% of total mass) in the ovary.

Amiodarone or various other iodine-containing medications can induce iodine-associated hyperthyroidism or thyrotoxicosis. This iodine-induced hyperthyroidism is described as the Jod-Basedow phenomena (Jod is the German word because that iodine).<2>

Risk Factors

The ubiquity of hyperthyroidism is different according to the ethnic team while in Europe, the frequency is affected by diet intake the Iodine, and also some cases are because of autoimmune disease. Subclinical hyperthyroidism occurs more in women older 보다 65 than in men, if overt hyperthyroidism rates are 0.4 every 1000 women and 0.1 per 1000 men and vary with age. 

Any evaluation of the an international epidemiology that hyperthyroidism will certainly delineate along the currently of iodine-sufficient regions and also iodine-deficient regions.<3> While iodine excess have the right to lead to hyperthyroidism, iodine deficiency deserve to lead to both hypothyroidism and also hyperthyroidism.

Graves disease is frequently seen in younger patients and is the many common cause of hyperthyroidism in that demographic. Toxicity multifocal goiter is generally seen in older individuals and also is the most common reason of hyperthyroidism in this corresponding demographic. Both Graves an illness and toxic multifocal goiter have a woman predilection and also are generally seen in patients v pertinent family and personal medical histories.

The 1977 Whickham inspection was an testimonial of the spectrum that thyroid obstacle in ar Durham in northeastern England. Although the demographics the the Whickham Survey included primary occupants of a community of northeastern England (and hence, negative extrapolation potential), the survey did present interesting results of hyperthyroidism. The Whickham survey demonstrated a pervasiveness of hyperthyroidism in women about 10-times an ext than the of guys (2.7% versus 0.23%).<4>


Hyperthyroidism might manifest together weight loss regardless of an increased appetite, palpitation, nervousness, tremors, dyspnea, fatigability, diarrhea or boosted GI motility, muscle weakness, warm intolerance, and diaphoresis. The signs and also symptoms that thyroid hormone exposure come peripheral tissues reflect a hypermetabolic state. A patient with hyperthyroidism classically presents v signs and also symptoms the reflect this state of enhanced metabolic activity. Usual symptoms the a patient might report encompass unintentional weight loss regardless of unchanged oral intake, palpitations, diarrhea or increased frequency of bowel movements, heat intolerance, diaphoresis, and/or term irregularities.

Physical check of the thyroid might or might not reveal an enlarged thyroid (goiter). The thyroid might be diffusely enlarged, or one or more nodules might be palpated. The thyroid might be painless come palpation or extremely tender to even light palpation.<5>


Thyroid stimulating hormone (TSH) is the early stage diagnostic test of choice and is considered the finest screening test for assessing the pathology the the thyroid and also for the surveillance of thyroid replacement therapy. As result of the an unfavorable feedback that T3 and also T4 exert ~ above the pituitary gland, elevated T3 and/or elevated T4 will reason decreased TSH production from the anterior pituitary gland. Abnormal TSH is often adhered to up v a measure up of complimentary T4 and/or cost-free T3.<6> concerns for an autoimmune procedure such as Graves an illness will warrant further evaluation by assessing serum levels of TSH-receptor antibodies.<7>

TSH level in the context of acute condition should be taken with more discretion as TSH levels room considerably more susceptible to the effects of illness.

Hyperthyroidism is a usual etiology because that atrial fibrillation; thus, more workup through an ECG may be warranted, particularly in a patience complaining the palpitations. Obtaining troponin levels is not regime unless the clinical presentation warrants additional cardiac ischemic workup, together as active chest pain.

Radiological diagnostics such as chest x-rays serve little diagnostic utility in the management of hyperthyroidism. Diagnostics such together ultrasound space not beneficial in diagnosing hyperthyroidism, yet the ultrasound result of nodules could potentially identify an etiology.

Since a majority of instances of hyperthyroidism are due to Graves disease or toxic multinodular goiter, confirmation of the diagnosis can be made based on history, clinical findings, and also palpating of the thyroid. In situations of diffusive goiter or no thyroid enlargement, a 24-hour radioactive iodine absorb (RAIU) is needed to distinguish between Graves condition and various other hyperthyroidism etiologies. Radioactive iodine uptake is the percentage of iodine-131 preserved by the thyroid ~ 24 hours. For the typical western diet, the normal variety of RAIU is frequently 10% come 30%.

Graves disease, toxicity multinodular goiter, and thyroid adenoma room etiologies the hyperthyroidism with increased RAIU, showing an enhanced synthesis the thyroid hormone. Subacute thyroiditis, painless thyroiditis, iodine-induced hyperthyroidism, and factitious hyperthyroidism have lessened RAIU. Thyroiditis to represent a disruption the the thyroid follicles through the subsequent release that thyroid hormone. Due to the fact that there is no boosted synthesis of thyroid hormone, RAIU will certainly be low in thyroiditis.<8>

If RAIU is not obtainable or is contraindicated, climate measurement that thyroid receptor antibodies deserve to be used as an alternative test because that diagnosis of tombs disease.<9>

A radioisotope thyroid scan is a diagnostic tool that utilizes technetium-99m pertechnetate together a radiation 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 together either "cold" (hypofunctioning), "warm" (isofunctioning), or "hot" (hyperfunctioning). "Cold" nodules raise problem for potential malignancy due to ineffective absorb of iodide and also synthesis of thyroid hormone typically seen in thyroid carcinomas.

Medical Management

Treatment of hyperthyroidism relies on the underlying etiology and also can be separated into 2 categories: symptomatic therapy and definitive therapy. The symptom of hyperthyroidism, such together palpitations, anxiety, and tremor, deserve to be controlled with a beta-adrenergic antagonist such together atenolol. Calcium channel blockers, such as verapamil, have the right to be offered as second-line therapy for patient who room beta-blocker intolerant or have contraindications come beta-blocker therapy.<10>

Transient creates of hyperthyroidism such together subacute thyroiditis or postpartum thyroiditis have to be managed with symptomatic therapy alone as the hyperthyroidism in this clinical cases tends to it is in self-limiting.

There room 3 definitive treatments of hyperthyroidism, all of which predispose the patient to potential long-term hypothyroidism: radioactive iodine therapy (RAI), thionamide therapy, and also subtotal thyroidectomy. Clinical assessment and also monitoring of free T4 space imperative because that patients who undergo any type of of these treatments. TSH-monitoring standing after definitive treatment is of poor utility because TSH stays suppressed until the patient i do not care euthyroid. Thus, TSH monitoring for thyroid condition is no recommended immediately adhering to definitive therapy.

The an option of i beg your pardon definitive treatment modality counts on the etiology. RAI treatment is considered the therapy of an option in nearly all patients v Graves an illness due to a high efficacy. In spite of the relative safety and also high efficacy, RAI is contraindicated in patient who room pregnant or patient who are breastfeeding.

In RAI therapy, radiation iodine-131 is administered v subsequent devastation of thyroid tissue. A single dose is adequate to manage hyperthyroidism in a far-reaching portion of patients, and the impacts of various other parts that the human body are basically negligible as result of the high thyroid absorb of the radioactive iodine-131. In a female patience of reproductive potential, that is highly recommended to acquire a beta-hCG to preeminence out pregnancy prior to initiation the RAI therapy. Any patient top top a thionamide (methimazole or propylthiouracil) have to be instructed come discontinue this therapy roughly 1 week before RAI therapy due to the fact that thionamide administration can interfere v the therapeutic advantage of RAI therapy. Number of months are typically needed standing post-RAI therapy to accomplish euthyroid status. Typically, patients room evaluated in 4 to 6-week intervals with raised time intervals because that stable, plasma-free T4 levels. Failure to attain euthyroidism ~ RAI therapy may indicate the need for one of two people repeat RAI therapy (for symptomatic hyperthyroidism) or the initiation of thyroxine treatment (for hypothyroidism).

RAI therapy involves the release of stored thyroid hormone, resulting in transient hyperthyroidism. This is normally well tolerated, although this transient hyperthyroidism is of worry in patient with far-ranging cardiac disease. For patients with cardiac disease, pretreatment v a thionamide to deplete the stored hormone is recommended to avoid the potential exacerbation the cardiac disease.

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

The establishment of a euthyroid status frequently requires numerous months after ~ initiation the thionamide therapy. Back methimazole and PTU are equally effective, methimazole is desired due come a relatively much better safety profile. An exemption to this reference is in pregnant patients, in i m sorry PTU is preferred. Methimazole is linked with an boosted risk of congenital defects, and thus PTU is wanted in the administration of gestational hyperthyroidism.

Side effects of thionamide therapy incorporate agranulocytosis, hepatitis, vasculitis, and also drug-induced lupus. Back these space rare side effects, patients have to be warned about the potential because that these next effects. Patient should additionally be recommend to discontinue the thionamide immediately and also notify their doctor if symptom suggestive the agranulocytosis happen (fever, chills, rapidly gradual infection, ill throat, amongst others). Regimen monitoring of leukocyte counts is not recommended when beginning a patient on a thionamide because of the fast onset of agranulocytosis. A baseline substantial metabolic dashboard (CMP) to evaluate hepatic condition would no be unreasonable due to the potential because that hepatitis.

Subtotal thyroidectomy is made use of for long-term regulate of hyperthyroidism. Preparation of the patient because that a subtotal thyroidectomy includes pretreatment through methimazole to achieve a virtually euthyroid status. Supersaturated potassium iodide is then included daily around 2 weeks before surgery and discontinued postoperatively. Alternatively, atenolol deserve to be began 1 to 2 weeks prior to surgery to minimize resting heart rate. Supersaturated potassium iodide is additionally dosed and discontinued postoperatively. The reason behind these management plans is to alleviate complications associated with perioperative exacerbation that hyperthyroidism.

See more: Words That Rhyme With He Near Rhymes, All Rhymes For He

Complications that subtotal thyroidectomy incorporate hypothyroidism as result of the decreased secretory potential that T4. Hypothyroidism remains the most usual complication linked with subtotal thyroidectomy. The proximity that the parathyroid glands come the thyroid gland can an outcome in the removal of parathyroid glands in addition to thyroid tissue, resulting in hypoparathyroidism. Due to the danger of iatrogenic injury come the recurrent laryngeal nerve, vocal cord paralysis is also a complication that subtotal thyroidectomy. All of these complications have to be questioned with the patient, and also the discussion should it is in documented.