At a glance......
- 1 Causes of Hyperthyroidism
- 2 Symptoms of Hyperthyroidism
- 3 Signs of Hyperthyroidism
- 4 Treatment
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Hyperthyroidism is the condition that occurs due to excessive production of thyroid hormone by the thyroid gland. Thyrotoxicosis is the condition that occurs due to excessive thyroid hormone of any cause and therefore includes hyperthyroidism. Some, however, use the terms interchangeably. Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat intolerance, diarrhea, enlargement of the thyroid, and weight loss. Symptoms are typically less in the old and during pregnancy. An uncommon complication is thyroid storm in which an event such as an infection results in worsening symptoms such as confusion and a high temperature and often results in death. The opposite is hypothyroidism when the thyroid gland does not make enough thyroid hormone
Causes of Hyperthyroidism
The major causes in humans are
- Graves’ disease. An autoimmune disease (usually, the most common etiology with 50-80% worldwide, although this varies substantially with location- i.e., 47% in Switzerland (Horst et al., 1987) to 90% in the USA (Hamburger et al. 1981)). Thought to be due to varying levels of iodine in the diet. It is eight times more common in females than males and often occurs in young females, around 20 – 40 years of age.
- Toxic thyroid adenoma (the most common etiology in Switzerland, 53%, thought to be atypical due to a low level of dietary iodine in this country)
- Toxic multinodular goiter
High blood levels of thyroid hormones (most accurately termed hyperthyroxinemia) can occur for a number of other reasons
- Inflammation of the thyroid is called thyroiditis. There are several different kinds of thyroiditis including Hashimoto’s thyroiditis (Hypothyroidism immune-mediated), and subacute thyroiditis (de Quervain’s). These may be initiallyassociated with secretion of excess thyroid hormone but usually progress to gland dysfunction and, thus, to hormone deficiency and hypothyroidism.
- Oral consumption of excess thyroid hormone tablets is possible (surreptitious use of thyroid hormone), as is the rare event of consumption of ground beef contaminated with thyroid tissue, and thus thyroid hormone (termed “hamburger hyperthyroidism”). Pharmacy compounding errors may also be a cause.
- Amiodarone, an antiarrhythmic drug, is structurally similar to thyroxine and may cause either under- or overactivity of the thyroid.
- Postpartum thyroiditis (PPT) occurs in about 7% of women during the year after they give birth. PPT typically has several phases, the first of which is hyperthyroidism. This form of hyperthyroidism usually corrects itself within weeks or months without the need for treatment.
- A struma ovarii is a rare form of monodermal teratoma that contains mostly thyroid tissue, which leads to hyperthyroidism.
- Excess iodine consumption notably from algae such as kelp.
Thyrotoxicosis can also occur after taking too much thyroid hormone in the form of supplements, such as levothyroxine (a phenomenon known as exogenous thyrotoxicosis, alimentary thyrotoxicosis, or occult factitial thyrotoxicosis).
Hypersecretion of thyroid stimulating hormone (TSH), which in turn is almost always caused by a pituitary adenoma, accounts for much less than 1 percent of hyperthyroidism cases.
Symptoms of Hyperthyroidism
|Constitutional||Weight loss, heat intolerance, perspiration|
|Cardiopulmonary||Palpitations, chest pain, dyspnea|
|Neuropsychiatric||Tremor, anxiety, double vision, muscle weakness|
|Neck||Fullness, dysphagia, dysphonia|
|Reproductive||Irregular menses, decreased libido, gynecomastia|
Signs of Hyperthyroidism
|Vital signs||Tachycardia, widened pulse pressure, fever|
|Cardiovascular||Hyperdynamic precordium, CHF, atrial fibrillation, systolic flow murmur|
|Ophthalmologic||Widened palpebral fissure, periorbital edema, proptosis, diplopia, restricted superior gaze|
|Neurologic||Tremor, hyperreflexia, proximal muscle weakness|
|Dermatologic||Palmar erythema, hyperpigmented plaques or non-pitting edema of tibia|
|Neck||Enlarged or nodular thyroid|
Symptoms of Hyperthyroidism
Generalized hypermetabolism from hyperthyroidism causes increased Na+/K+-ATPase to promote thermogenesis. There is increased catecholamine secretion and, beta-adrenergic receptors are also upregulated in various tissues. As a result of the hyperadrenergic state, peripheral vascular resistance is decreased. In the heart, hyperthyroidism causes a decreased amount of phospholamban, a protein that normally decreases the affinity of calcium-ATPase for calcium in the sarcoplasmic reticulum. As a result of decreased phospholamban, there is increased Ca+ movement between the sarcoplasmic reticulum and cytosol, leading to increased contractility. Increased beta-receptors on the heart also leads to increased cardiac output.
Increased sweating from cutaneous blood flow increase
Onycholysis (separation of nails from nail beds)
Lid lag (when looking down, sclera visible above cornea)
Lid retraction (when looking straight, sclera visible above the cornea)
Diffuse, smooth, non-tender goiter
The audible bruit can be heard at the superior poles
Tachycardia (can be masked by patients taking beta-blockers)
An irregular pulse from atrial fibrillation
Widened pulse pressure because systolic pressure increases and diastolic pressure decreases
Heart failure (elderly patients)
Abnormal heart rhythms
Fine tremors of the outstretched fingers. Face, tongue, and head can also be involved. Tremors respond well to treatment with beta-blockers.
Myopathy affecting proximal muscles. Serum creatine kinase levels can be normal
Osteoporosis caused by the direct effects of T3. Elderly patients can present with fractures.
Conditions associated with hypothyroidism
Conditions associated with hyperthyroidism
Thyrotropic pituitary adenoma
Drug-induced: amiodarone, lithium
Thyrotoxicosis and thyroid storm
Toxic multinodular goiter [rx]
Thyroid adenoma [rx]
Antithyroid drugs that work in the thyroid gland
Perchlorate – inhibits Na+/I- symporter – blocks iodide uptake
Thionamides – inhibits TPO – block thyroid hormone synthesis
Iodide > 5mg – inhibits Na+/I- symporter and TPO – blocks iodide uptake and thyroid hormone synthesis
Lithium – inhibits thyroid hormone release (off-label use for thyroid storm)
Antithyroid drugs that work in peripheral tissue – all these drugs inhibit the deiodinase enzymes. Deiodinase enzymes normally convert T4 into the active form T3. These drugs inhibit the conversion of T4 to T3 and reduce its activity.
Scoring (Burch, Wartofsky)
|Moderate (rales, atrial fibrillation)||10|
|Nausea/vomiting, abdominal pain||10|
- >45: thyroid storm
- 25-44: impending thyroid storm
- <25: unlikely thyroid storm
- Supportive measures
- Volume resuscitation and cooling
- Benzodiazepines for agitation
- Propranolol 60-80mg PO q4h
- Propranolol 0.5-1.0mg IV, repeat q15min then 1-2mg q3h
- Esmolol continuous infusion
- Endocrinology consultation
- PTU, SSKI
Thyrostatics (antithyroid drugs) are drugs that inhibit the production of thyroid hormones, such as carbimazole (used in the UK) and methimazole (used in the US, Germany and Russia), and propylthiouracil. Thyrostatics are believed to work by inhibiting the iodination of thyroglobulin by thyroperoxidase and, thus, the formation of tetraiodothyronine (T4). Propylthiouracil also works outside the thyroid gland, preventing the conversion of (mostly inactive) T4 to the active form T3. Because thyroid tissue usually contains a substantial reserve of thyroid hormone, thyrostatics can take weeks to become effective and the dose often needs to be carefully titrated over a period of months, with regular doctor visits and blood tests to monitor results.
Many of the common symptoms of hyperthyroidism such as palpitations, trembling, and anxiety is mediated by increases in beta-adrenergic receptors on cell surfaces. Beta blockers, typically used to treat high blood pressure, are a class of drugs that offset this effect, reducing rapid pulse associated with the sensation of palpitations, and decreasing tremor and anxiety.
Some minimal effect on thyroid hormone production however also comes with Propranolol – which has two roles in the treatment of hyperthyroidism, determined by the different isomers of propranolol. L-propranolol causes beta-blockade, thus treating the symptoms associated with hyperthyroidism such as tremor, palpitations, anxiety, and heat intolerance. D-propranolol inhibits thyroxine deiodinase, thereby blocking the conversion of T4 to T3, providing some though minimal therapeutic effect. Other beta-blockers are used to treat only the symptoms associated with hyperthyroidism. Propranolol in the UK, and Metoprolol in the US, are most frequently used to augment treatment for hyperthyroid patients.
People with autoimmune hyperthyroidism should not eat foods high in iodine, such as edible seaweed and kelps.
From a public health perspective, the general introduction of iodized salt in the United States in 1924 resulted in lower disease, goiters, as well as improving the lives of children whose mothers would not have eaten enough iodine during pregnancy which would have lowered the IQs of their children.
Surgery (thyroidectomy to remove the whole thyroid or a part of it) is not extensively used because most common forms of hyperthyroidism are quite effectively treated by the radioactive iodine method, and because there is a risk of also removing the parathyroid glands, and of cutting the recurrent laryngeal nerve, making swallowing difficult, and even simply generalized staphylococcal infection as with any major surgery. Some people with Graves’ may opt for surgical intervention. This includes those that cannot tolerate medicines for one reason or another, people that are allergic to iodine, or people that refuse radioiodine.
If people have toxic nodules treatments typically include either removal or injection of the nodule with alcohol.
In iodine-131 (radioiodine) radioisotope therapy, which was first pioneered by Dr. Saul Hertz, radioactive iodine-131 is given orally (either by pill or liquid) on a one-time basis, to severely restrict, or altogether destroy the function of a hyperactive thyroid gland. This isotope of radioactive iodine used for ablative treatment is more potent than diagnostic radioiodine (usually iodine-123 or a very low amount of iodine-131), which has a biological half-life from 8–13 hours. Iodine-131, which also emits beta particles that are far more damaging to tissues at short range, has a half-life of approximately 8 days. Patients not responding sufficiently to the first dose are sometimes given an additional radioiodine treatment, at a larger dose. Iodine-131 in this treatment is picked up by the active cells in the thyroid and destroys them, rendering the thyroid gland mostly or completely inactive