Sandbox: hyperthyroidism
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Hyperthyroidism |
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Hyperthyroidism On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Jinhui Wu, M.D.
Overview
Hyperthyroidism is a disorder that the thyroid gland makes too much thyroid hormone. About 1 percent of the U.S. population has hyperthyroidism. Some diseases, such as Graves’ disease, thyroid nodules and thyroiditis, are associated with the cause of hyperthyroidism. Hyperthyroidism can affect your metabolism. Usual signs and symptoms include goiter, increased appetite but weight loss, palpitation, hypertension, increased sensitivity to heat and perspiration, nervousness and hand tremors. The Thyroid-Stimulating Hormone (TSH) test is a very sensitive and useful test to identify the disorder. Other examinations include the T3 and T4 test, radioactive iodine uptake test and thyroid scan. Treatment options of hyperthyroidism depends on the cause, age, physical condition and the severity of symptoms. Usual treatment measures are medications, radioactive iodine and thyroidectomy. The common side effect of radioactive iodine and thyroidectomy is hypothyroidism. The patient will need to take thyroid hormone supplement to restore normal hormone levels.
What are the symptoms of Hyperthyroidism?
Symptoms of hyperthyroidism vary from person to person. Usual signs include the following:
- Goiter
- Increased appetite, but weight loss
- Palpitation
- Hypertension
- Increased sensitivity to heat and perspiration
- Nervousness, anxiety or irritability, difficulty sleeping
- Hand tremors
- Fatigue, muscle weakness
- Changes in menstrual patterns (usually lighter flow, less frequent periods) in women
Other health problems may also cause these symptoms. Only a doctor can tell for sure. A person with any of these symptoms should tell the doctor so that the problems can be diagnosed and treated as early as possible.
Who is at highest risk?
- Graves’ disease
- Thyroid nodules
- Thyroiditis
- Too much iodine ingestion
- Over-medicating with synthetic thyroid hormone
Diagnosis
- Thyroid-Stimulating Hormone (TSH) test: This is a very sensitive and useful test and usually used as the first test to identify the disorder. The TSH test is based on the feedback between TSH and thyroid hormone. Patients with hyperthyroidism may show a lower reading than normal people.
- T3 and T4 test: This test may show the levels of T3 and T4 in your blood. In patients with hyperthyroidism, the levels of one or both of these hormones in your blood will be higher than normal.
- Thyroid-stimulating immunoglobulin (TSI) test: This test may help diagnose Graves' disease, which has this kind of antibody.
- Radioactive iodine uptake test: This test can detect the iodine uptake function of your thyroid gland and help diagnose the cause of hyperthyroidism. For example, low levels of iodine uptake might be a sign of thyroiditis, whereas high levels could indicate Graves’ disease.
- Thyroid scan: This test may also help diagnose the cause of hyperthyroidism by providing images of nodules and other possible thyroid irregularities.
Other diseases with similar symptoms:
- Autonomic nerve dysfunction
- Coronary artery disease
- Goiter
- Schizophrenia
- Thyroid cancer
When to seek urgent medical care?
Call your health care provider if symptoms of hyperthyroidism develop. If you experience either of the following symptoms, seeking urgent medical care as soon as possible:
- Palpitation
- Severe hypertension
Treatment options
Usual treatment measures of hyperthyroidism include medications, radioactive iodine, and surgery. Treatment options depends on the cause, age, physical condition and the severity of symptoms.
- Medications: Antithyroid medications, such as methimazole (Tapazole) and propylthiouracil (PTU), are used to block the production of thyroid hormone. Symptoms may begin to improve in 6 to 12 weeks and the whole treatment period may last for at least a year. Beta blockers, for example propranolol, may be used to relieve symptoms such as palpitation, nervousness,hypertension, sweating and shaking.
- Radioactive iodine: This kind of treatment may destroy the thyroid gland and stop the excess production of hormones. During this period, the patient takes radioactive iodine by mouth. A common side effect is permanent hypothyroidism, which needs thyroid supplements.
- Surgery: Thyroidectomy is another type of treatment option. The possible side effect after surgery is hypothyroidism. Patients need to take thyroid hormone supplements to restore normal hormone levels.
Contraindicated medications
Patients diagnosed with hyperthyroidism should avoid using the following medications:
- Levothyroxine
- Phentermine
If you have been diagnosed with hyperthyroidism, consult your physician before starting or stopping any of these medications.
Where to find medical care for Hyperthyroidism?
Directions to Hospitals Treating Hyperthyroidism
Prevention
- For hyperthyroidism caused by too much iodine ingestion, the method of prevention is decreasing iodine ingestion and a regular check of thyroid hormone levels in the blood.
- For hyperthyroidism caused by over-medicating with synthetic thyroid hormone, giving the appropriate dose to patients and a regular check of thyroid hormone levels in the blood may be important.
What to expect (Outlook/Prognosis)?
Many cases of hyperthyroidism are generally treatable. Prognosis depends on whether or not the patient has severe complications.
Possible Complications
Sources
- http://www.endocrine.niddk.nih.gov/pubs/Hyperthyroidism/
- http://www.nlm.nih.gov/medlineplus/ency/article/000356.htm
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Overview
Hyperthyroidism is the clinical syndrome caused by an excess of circulating free thyroxine (T4) or free triiodothyronine (T3), or both.
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Hyperthyroidism from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Minor ocular signs, which may be present in any type of hyperthyroidism, are eyelid retraction ("stare") and lid-lag. These "fear-like" eye-signs result from thyroid hormone's exacerbation of the action of norepinephrine. In hyperthyroid stare (Dalrymple sign) the eyelids are retracted upward more than normal (the normal position is at the superior corneoscleral limbus, where the "white" of the eye begins at the upper border of the iris). In lid-lag (von Graefe's sign), when the patient tracks an object downward with their eyes, the eyelid fails to follow the downward moving iris, and the same type of upper globe exposure which is seen with lid retraction occurs, temporarily. These signs disappear with treatment of the hyperthyroidism, or treatment by certain anti-adrenergic drugs.
Laboratory Findings
A diagnosis is suspected through blood tests, by measuring the level of thyroid-stimulating hormone (TSH) in the blood. A low TSH (the job of TSH taken over by thyroid-stimulating immunoglobulin [TSI] that act like TSH) indicates increased levels of T4 and/or T3 in the blood. Measuring specific antibodies, such as anti-TSH-receptor antibodies in Graves' disease, may contribute to the diagnosis.
Electrocardiogram
Chest X Ray
CT
MRI
Echocardiography or Ultrasound
Other Imaging Findings
In all patients with hyperthyroxinemia, scintigraphy is required in order to distinguish true hyperthyroidism from thyroiditis.
Other Diagnostic Studies
Treatment
Medical Therapy
The major and generally accepted modalities for treatment of hyperthyroidism in humans involve initial temporary use of suppressive thyrostatics medication, and possibly later use of permanent surgical or radioisotope therapy. All approaches may cause under active thyroid function (hypothyroidism) which is easily managed with levothyroxine supplementation.
Surgery
Surgery as an option predates the use of the less invasive radioisotope therapy, but is still required in cases where the thyroid gland is enlarged and causing compression to the neck structures, or the underlying cause of the hyperthyroidism may be cancerous in origin.
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]
Overview
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Historical Perspective
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4] Farman Khan, MD, MRCP [5]
Overview
Classification
- Graves' disease: An autoimmune disorder resulting from thyroid-stimulating immunoglobulins, which stimulate thyroid gland growth and hormone synthesis. It's prominent features, including pretibial myxedema and ophthalmopathy, are autoimmune in origin. Graves' disease is the most common cause of hyperthyroidism.[1] High iodine intake and stressful events may be risk factors.
- Toxic adenoma and toxic multinodular goiter: It results from focal or diffuse hyperplasia of thyroid follicular cells which are independent of regulation by TSH. Activating somatic mutations of the genes for the TSH receptor have been found in both of these. Mutations of the TSH-receptor gene are most common; they were found in 15 of 31 toxic adenomas in one study.[2]
- Hashitoxicosis: It has two phases, initially it presents with hyperthyroidism and a high radioiodine uptake caused by TSH-receptor antibodies. This is followed by infiltration of the gland with lymphocytes resulting in autoimmune-mediated destruction of thyroid tissue leading to the development of hypothyroidism.
- Iodine-induced hyperthyroidism: Develop after an iodine load or iodine-rich drugs such as amiodarone.
- TSH-mediated hyperthyroidism: It is because of increased TSH production. It has two forms, neoplastic and non-neoplastic. Neoplastic includes TSH-producing pituitary adenoma. Almost all of these patients have a goiter, 40 percent have defects in their field of vision, and one-third of women have galactorrhea. All patients have high serum thyroid hormone concentrations. Non-neoplastic TSH-mediated hyperthyroidism is due to resistance of the effect of thyroid hormone on pituitary TSH.
- Trophoblastic disease and germ cell tumors: Hyperthyroidism can occur in women with a hydatidiform mole or choriocarcinoma and in men with testicular germ cell tumors.
References
- ↑ Brent GA (2008). "Clinical practice. Graves' disease". The New England Journal of Medicine. 358 (24): 2594–605. doi:10.1056/NEJMcp0801880. PMID 18550875. Unknown parameter
|month=ignored (help) - ↑ Führer D, Holzapfel HP, Wonerow P, Scherbaum WA, Paschke R (1997). "Somatic mutations in the thyrotropin receptor gene and not in the Gs alpha protein gene in 31 toxic thyroid nodules". J. Clin. Endocrinol. Metab. 82 (11): 3885–91. PMID 9360556. Unknown parameter
|month=ignored (help)
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [6] Farman Khan, MD, MRCP [7]
Overview
Pathophysiology
Thyroid hormone secretions are controlled by complex hypothalamic-pituitary-thyroid axis. Under normal circumstances thyrotropin-releasing hormone (TRH) from the hypothalamus stimulates the pituitary to release TSH. TSH in return acts on thyroid to produce T3 and T4. In turn, these hormones act on the hypothalamus to decrease TRH secretion and thus the synthesis of TSH. Iodine is essential for the synthesis of thyroid hormone. Dietary inorganic iodide is transported into the gland and then converted to iodine. Iodine binds to thyroglobulin with the help of thyroid peroxidase by process called organification. This forms monoiodotyrosine (MIT) and diiodotyrosine (DIT), which are coupled to form T3 and T4; these are then stored with thyroglobulin in the thyroid’s follicular lumen. More than 99% of T3 and T4 is bound to plasma proteins in the peripheral circulation and is inactive. Free T3 is 20-100 times more biologically active than free T4. Free T3 acts by binding to nuclear receptors and regulating the transcription of various cellular proteins. Any process that increases unbound thyroid hormone in peripheral circulation can cause hyperthyroidism. Disturbances of the thyroid axis can occur at the level of the hypothalamus, pituitary gland, thyroid gland, or in the periphery. Hyperthyroidism results in an increase in the transcription of cellular proteins, causing an increased basal metabolic rate.
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [8] Associate Editor(s)-in-Chief: Vignesh Ponnusamy, M.B.B.S. [9] Luke Rusowicz-Orazem, B.S.
Overview
Hyperthyroidism is the result of excess thyroid hormone production, causing an overactive metabolism and increased speed of all the body's processes.
Thyroid hormone generally controls the pace of all of the processes in the body. This pace is called one's metabolism. If there is too much thyroid hormone, every function of the body tends to speed up. The thyroid gland regulates the body temperature by secreting two hormones that control how quickly the body burns calories and energy. If the thyroid produces too much hormone, the condition is called hyperthyroidism, but if too little is produced, the result is hypothyroidism.
Causes
Major causes in humans are:
Other causes of hyperthyroxinemia (high blood levels of thyroid hormones) are not to be confused with true hyperthyroidism and include subacute and other forms of thyroiditis (inflammation) and struma ovarii (a teratoma). Thyrotoxicosis (symptoms caused by hyperthyroxinemia) can occur in both hyperthyroidism and thyroiditis. When it causes acutely increased metabolism, it is sometimes called "thyroid storm", a life-threatening event characterized by tachycardia, hypertension, and fever.
Excess thyroid hormone from pills can also cause hyperthyroidism. Amiodarone, a heart medication, can sometimes cause hyperthyroidism. Hamburger toxicosis is a condition that occurs sporadically and is associated with ground beef contaminated with thyroid hormone.
Postpartum thyroiditis occurs in about 7% of women during the year after they give birth. PPT typically has several phases, the first of which is hyperthyroidism. Many times, the hyperthyroidism corrects itself within weeks or months without any treatment necessary.
Life Threatening Causes
- Adenocarcinoma
- Choriocarcinoma
- Metastatic follicular thyroid cancer
- Pituitary tumor
- Struma ovarii
- Teratoma
- Testicular cancer
- Thyroid adenoma
- Thyroid carcinoma
- Thyroid nodule
- Thyroid tumor
- Thyrotropinoma
- Toxic adenoma
- Toxic thyroid adenoma
- Trophoblastic disease
- Tsh-producing pituitary adenoma
Common Causes
Causes by Organ System
Causes in Alphabetical Order
- Adenocarcinoma
- Amiodarone
- Anterior pituitary hyperhormonotrophic syndrome
- Atezolizumab
- Autoimmune enteropathy
- Autoimmune thyroid disease
- Autonomous thyroid tissue
- Choriocarcinoma
- De quervain thyroiditis
- Diabetes mellitus
- Diarrhea
- Enteropathy
- Excessive replacement therapy
- Exogenous thyroid hormone intake
- Factitious thyroiditis
- Glutaricaciduria type 3
- Graves' disease
- Hashimoto's thyroiditis
- Hashitoxicosis
- Hydatidiform mole
- Hyperemesis gravidarum
- Immune dysregulation
- Intentional suppressive therapy
- Iodine overuse
- Ipex syndrome
- Jod-basedow thyrotoxicosis
- Levothyroxine and indinavir interaction
- Mccune-albright syndrome
- Metastatic follicular thyroid cancer
- Nivolumab
- Pituitary tumor
- Poems syndrome
- Polyendocrinopathy
- Polyostotic fibrous dysplasia
- Postpartum thyroiditis
- Potassium iodide
- Pramipexole
- Sorafenib
- Struma ovarii
- Suppurative thyroiditis
- Teratoma
- Testicular cancer
- Thyroid adenoma
- Thyroid carcinoma
- Thyroid nodule
- Thyroid stimulating globulin
- Thyroid tumor
- Thyroiditis
- Thyrotoxicosis factitia
- Thyrotropinoma
- Thyroxine
- Toxic adenoma
- Toxic multinodular goiter
- Toxic thyroid adenoma
- Troell-junet syndrome
- Trophoblastic disease
- Tsh hypersecretion
- Tsh-mediated hyperthyroidism
- Tsh-producing pituitary adenoma
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [10]
Overview
Differentiating Hyperthyroidism from other Diseases
- Amiodarone
- Gestational thyrotoxicosis
- Grave's Disease
- Hashimoto's thyroiditis
- HCG-secreting tumors
- Iatrogenic factitious
- Iodine excess
- Metastatic differentiated thyroid cancer
- Radiation thyroiditis
- Reidel's thyroiditis
- Silent thyroiditis
- Struma ovarii
- Subacute thyroiditis
- Suppurative thyroiditis
- Thyroid carcinoma
- Thyroid hormone resistance syndrome
- Toxic thyroid adenoma
- Toxic multinodular goiter
- TSH (thyroid stimulating hormone)-secreting pituitary adenoma
The table below summarizes the findings that differentiate watery causes of chronic diarrhea[1][2][3][4]
| Cause | Osmotic gap | History | Physical exam | Gold standard | Treatment | |||
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| < 50 mOsm per kg | > 50 mOsm per kg* | |||||||
| Watery | Secretory | Crohns | + | - |
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| Hyperthyroidism | + | - |
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| VIPoma | + | - |
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| Osmotic | Lactose intolerance | - | + |
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| Celiac disease | - | + |
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| Functional | Irritable bowel syndrome | - | - |
Abdominal pain or discomfort recurring at least 3 days per month in the past 3 months and associated with 2 or more of the following:
History of straining is also common |
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References
- ↑ Silverberg MS, Satsangi J, Ahmad T, Arnott ID, Bernstein CN, Brant SR; et al. (2005). "Toward an integrated clinical, molecular and serological classification of inflammatory bowel disease: report of a Working Party of the 2005 Montreal World Congress of Gastroenterology". Can J Gastroenterol. 19 Suppl A: 5A–36A. PMID 16151544.
- ↑ Sauter GH, Moussavian AC, Meyer G, Steitz HO, Parhofer KG, Jüngst D (2002). "Bowel habits and bile acid malabsorption in the months after cholecystectomy". Am J Gastroenterol. 97 (7): 1732–5. doi:10.1111/j.1572-0241.2002.05779.x. PMID 12135027.
- ↑ Maiuri L, Raia V, Potter J, Swallow D, Ho MW, Fiocca R; et al. (1991). "Mosaic pattern of lactase expression by villous enterocytes in human adult-type hypolactasia". Gastroenterology. 100 (2): 359–69. PMID 1702075.
- ↑ RUBIN CE, BRANDBORG LL, PHELPS PC, TAYLOR HC (1960). "Studies of celiac disease. I. The apparent identical and specific nature of the duodenal and proximal jejunal lesion in celiac disease and idiopathic sprue". Gastroenterology. 38: 28–49. PMID 14439871.
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [11] Associate Editor(s)-in-Chief: Farman Khan, MD, MRCP [12]
Overview
Epidemiology and Demographics
Prevalence and Age
The overall prevalence of hyperthyroidism is around 1.3 percent, it increases to 5 percent in older women. [1] 60-80% of the cases of thyrotoxicosis in the United States are caused by Graves' disease. The incidence of Graves' disease has been reported to be 50 cases per 100,000 people, with the peak occurrence in ages 20-40 years. Toxic multinodular goiters occur in patients with a long history of nontoxic goiter and therefore are usually present after 50 years of age. Patients with toxic adenomas present at a younger age than do patients with toxic multinodular goiter.
Sex
Hyperthyroidism is more common in women than men (5:1 ratio). Toxic nodular goiter is more common in older women, while Graves' disease is seen most often in younger women. Graves ophthalmopathy is more common in women than in men.
Race
Autoimmune thyroid disease occurs with the same frequency in Caucasians, Hispanics, and Asians but at lower rates in African Americans. Hyperthyroidism is also more common in smokers. [2]
References
- ↑ Hollowell JG, Staehling NW, Flanders WD, Hannon WH, Gunter EW, Spencer CA, Braverman LE (2002). "Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III)". The Journal of Clinical Endocrinology and Metabolism. 87 (2): 489–99. PMID 11836274. Unknown parameter
|month=ignored (help) - ↑ Asvold BO, Bjøro T, Nilsen TI, Vatten LJ (2007). "Tobacco smoking and thyroid function: a population-based study". Archives of Internal Medicine. 167 (13): 1428–32. doi:10.1001/archinte.167.13.1428. PMID 17620538. Unknown parameter
|month=ignored (help)
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [13], Farman Khan, MD, MRCP [14]
Overview
Risk Factors
Autoimmune disorders
A history of other autoimmune diseases like adrenal insufficiency and pernicious anemia increases the risk of hyperthyroidism.
Age
Hyperthyroidism can happen at any age, but it is more common in people aged 60 and older. Graves' disease is more common between 40-60 years of age.
Gender
Hyperthyroidism is more common in women than men.
Genetic Factors
A family history of Graves' disease or other forms of hyperthyroidism increases the risk of hyperthyroidism.
Race
Japanese people appear to be at a greater risk of hyperthyroidism.
Others
Other Factors like common viral infection and pregnancy may also increase the risk of hyperthyroidism.
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [15]
Overview
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Screening
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [16]
Overview
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Natural History
Complications
Prognosis
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [17]
Overview
History
Symptoms
Major clinical weight loss (often accompanied by a ravenous appetite), intolerance to heat, fatigue, weakness, hyperactivity, irritability, apathy, depression, polyuria, polydipsia, and sweating. Additionally, patients may present with a variety of symptoms such as palpitations and arrhythmias (notably atrial flutter or atrial fibrillation), shortness of breath (dyspnea), loss of libido, nausea, vomiting, and diarrhea. In the elderly, these classical symptoms may not be present and they may present only with fatigue and weight loss leading to apathetic hyperthyroidism.
Neurological manifestations are tremor, chorea, myopathy, and periodic paralysis. Stroke of cardioembolic origin due to coexisting atrial fibrillation may be mentioned as one of the most serious complications of hyperthyroidism.
As to other autoimmune disorders related with thyrotoxicosis, an association between thyroid disease and myasthenia gravis has been well recognized. The thyroid disease, in this condition, is often an autoimmune one and approximately 5% of patients with myasthenia gravis also have hyperthyroidism. Myasthenia gravis rarely improves after thyroid treatment and the relationship between the two entities is as yet unknown. Some very rare neurological manifestations that are reported to be dubiously associated with thyrotoxicosis are pseudotumor cerebri, amyotrophic lateral sclerosis and a Guillain-Barré-like syndrome.
Exophthalmos or (protrusion of the eyeball) occurs in Graves' disease, but it is not caused by the hyperthyroid state in that disease, and is unrelated to it. Exophthalmos, when present, may exacerbate ocular signs, however.[1]
References
- ↑ Faculty of Medicine & Dentistry (2006). "Course-Based Physical Examination - Endocrinology -- Endocrinology Objectives (Thyroid Exam)". Undergraduate Medical Education. University of Alberta. Retrieved 2007-01-28.
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [18]
Overview
Minor ocular signs, which may be present in any type of hyperthyroidism, are eyelid retraction ("stare") and lid-lag. These "fear-like" eye-signs result from thyroid hormone's exacerbation of the action of norepinephrine. In hyperthyroid stare (Dalrymple sign) the eyelids are retracted upward more than normal (the normal position is at the superior corneoscleral limbus, where the "white" of the eye begins at the upper border of the iris). In lid-lag (von Graefe's sign), when the patient tracks an object downward with their eyes, the eyelid fails to follow the downward moving iris, and the same type of upper globe exposure which is seen with lid retraction occurs, temporarily. These signs disappear with treatment of the hyperthyroidism, or treatment by certain anti-adrenergic drugs.
Physical Examination
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Skin
Vitiligo may be present in some patients
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [19]
Overview
A diagnosis is suspected through blood tests, by measuring the level of thyroid-stimulating hormone (TSH) in the blood. A low TSH (the job of TSH taken over by thyroid-stimulating immunoglobulin [TSI] that act like TSH) indicates increased levels of T4 and/or T3 in the blood. Measuring specific antibodies, such as anti-TSH-receptor antibodies in Graves' disease, may contribute to the diagnosis.
Laboratory Findings
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References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [20]
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Overview
Electrocardiogram
References
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Hashimoto's thyroiditis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Sandbox: hyperthyroidism On the Web |
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American Roentgen Ray Society Images of Sandbox: hyperthyroidism |
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Risk calculators and risk factors for Sandbox: hyperthyroidism |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [21]
Overview
Chest X Ray
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [22]
Overview
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Key CT Findings for Hyperthyroidism
Examples of CT Findings for Hyperthyroidism
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [23]
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Overview
Key MRI Findings for Hyperthyroidism
Examples of MRI Findings for Hyperthyroidism
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [24]
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Overview
Echocardiography or Ultrasound
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [25]
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Overview
In all patients with hyperthyroxinemia, scintigraphy is required in order to distinguish true hyperthyroidism from thyroiditis.
Other Imaging Findings
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [26]
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Overview
Other Diagnostic Studies
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [27]
Overview
The major and generally accepted modalities for treatment of hyperthyroidism in humans involve initial temporary use of suppressive thyrostatics medication, and possibly later use of permanent surgical or radioisotope therapy. All approaches may cause under active thyroid function (hypothyroidism) which is easily managed with levothyroxine supplementation.
Medical Therapy
Thyrostatics
Thyrostatics are drugs that inhibit the production of thyroid hormones, such as carbimazole (used in UK) and methimazole (used in US), or where these are not tolerated then propylthiouracil is used. Thyrostatics are believed to work by inhibiting the iodination of thyroglobulin by thyroperoxidase.
If too high a dose is used in pharmacological treatment, patients can develop symptoms of hypothyroidism.
Beta-blockers
Beta-blockers do not treat, but rather mask, common symptoms of hyperthyroidism such as palpitations, trembling, and anxiety. Propranolol in the UK, and Metoprolol in the US, are most frequently used to augment treatment for hyperthyroid patients.
Radio-active Iodine
In Iodine-131 (Radioiodine) Radioisotope Therapy, radio-active iodine is given orally (either by pill or liquid) on a one-time basis to destroy the function of a hyperactive gland. The iodine given for ablative treatment is different from the iodine used in a scan. Radio-active iodine is given after a routine iodine scan, and uptake of the iodine is determined to confirm hyperthyroidism. The radio-active iodine is picked up by the active cells in the thyroid and destroys them. Since iodine is only picked up by thyroid cells (and picked up more readily by over-active thyroid cells), the destruction is local, and there are no widespread side effects with this therapy. Radio-active iodine ablation has been safely used for over 50 years, and the only major reasons for not using it are pregnancy and breast-feeding.
Often, due to the difficulty of picking the correct dose, the treatment results in an opposite condition - hypothyroidism. This is considered uncommon since the radioiodine has more affinity towards over-active thyroid cells than it does for the normal ones.
Contraindicated medications
Hyperthyroidism is considered an absolute contraindication to the use of the following medications:
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [28]
Overview
Surgery as an option predates the use of the less invasive radioisotope therapy, but is still required in cases where the thyroid gland is enlarged and causing compression to the neck structures, or the underlying cause of the hyperthyroidism may be cancerous in origin.
Surgery
Surgery (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. However, some Graves' disease patients who cannot tolerate medicines for one reason or another, patients who are allergic to iodine, or patients who refuse radioiodine opt for surgical intervention. Also, some surgeons believe that radioiodine treatment is unsafe in patients with an unusually large gland, or those whose eyes have begun to bulge from their sockets, claiming that the massive dose of iodine needed will only exacerbate the patient's symptoms. The procedure is quite safe - some surgeons even perform partial thyroidectomies on an out-patient basis.
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [29]
Overview
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Primary Prevention
References
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Hyperthyroidism Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [30]
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