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|Diffuse hyperplasia of the thyroid|
A goitre, associated with hypothyroidism or hyperthyroidism, may be present with symptoms of the underlying disorder. For hyperthyroidism, the most common symptoms are associated with adrenergic stimulation: tachycardia (increased heart rate), palpitations, nervousness, tremor, increased blood pressure and heat intolerance. Clinical manifestations are often related to hypermetabolism, (increased metabolism), excessive thyroid hormone, an increase in oxygen consumption, metabolic changes in protein metabolism, immunologic stimulation of diffuse goitre, and ocular changes (exophthalmos). Hypothyroid individuals may have weight gain despite poor appetite, cold intolerance, constipation and lethargy. However, these symptoms are often non-specific and make diagnosis difficult.
Regarding morphology, goitres may be classified either as the growth pattern or as the size of the growth:
Goitre with autonomous adenoma
Worldwide, the most common cause for goitre is iodine deficiency, usually seen in countries that do not use iodized salt. Selenium deficiency is also considered a contributing factor. In countries that use iodized salt, Hashimoto's thyroiditis is the most common cause. Goitre can also result from cyanide poisoning; this is particularly common in tropical countries where people eat the cyanide-rich cassava root as the staple food.
|Cause||Pathophysiology||Resultant thyroid activity||Growth pattern||Treatment||Incidence and prevalence||Prognosis|
|Iodine deficiency||Hyperplasia of thyroid to compensate for decreased efficacy||Can cause hypothyroidism||Diffuse||Iodine||Constitutes over 90% cases of goitre worldwide||Increased size of thyroid may be permanent if untreated for around five years|
|Congenital hypothyroidism||Inborn errors of thyroid hormone synthesis||Hypothyroidism|
|Adverse drug reactions|
|Hashimoto's thyroiditis||Autoimmune disease in which the thyroid gland is gradually destroyed. Infiltration of lymphocytes.||Hypothyroidism||Diffuse and lobulated||Thyroid hormone replacement||Prevalence: 1 to 1.5 in a 1000||Remission with treatment|
|Pituitary disease||Hypersecretion of thyroid stimulating hormone, almost always by a pituitary adenoma||Diffuse||Pituitary surgery||Very rare|
|Graves' disease—also called Basedow syndrome||Autoantibodies (TSHR-Ab) that activate the TSH-receptor (TSHR)||Hyperthyroidism||Diffuse||Antithyroid agents, radioiodine, surgery||Will develop in about 0.5% of males and 3% of females||Remission with treatment, but still lower quality of life for 14 to 21 years after treatment, with lower mood and lower vitality, regardless of the choice of treatment|
|Thyroiditis||Acute or chronic inflammation||Can be hyperthyroidism initially, but progress to hypothyroidism|
|Thyroid cancer||Usually uninodular||Overall relative 5-year survival rate of 85% for females and 74% for males|
|Benign thyroid neoplasms||Usually hyperthyroidism||Usually uninodular||Mostly harmless|
|Thyroid hormone insensitivity||Secretional hyperthyroidism,
Goitre is treated according to the cause. If the thyroid gland is producing too much T3 and T4, radioactive iodine is given to the patient to shrink the gland. If goitre is caused by iodine deficiency, small doses of iodide in the form of Lugol's Iodine or KI solution are given. If the goitre is associated with an underactive thyroid, thyroid supplements are used as treatment. In extreme cases, a partial or complete thyroidectomy is required.
Goitre is more common among women, but this includes the many types of goitre caused by autoimmune problems, and not only those caused by simple lack of iodine.
Chinese physicians of the Tang Dynasty (618–907) were the first to successfully treat patients with goitre by using the iodine-rich thyroid gland of animals such as sheep and pigs—in raw, pill, or powdered form. This was outlined in Zhen Quan's (d. 643 AD) book, as well as several others. One Chinese book, The Pharmacopoeia of the Heavenly Husbandman, asserted that iodine-rich sargassum was used to treat goitre patients by the 1st century BC, but this book was written much later.
In the 12th century, Zayn al-Din al-Jurjani, a Persian physician, provided the first description of Graves' disease after noting the association of goitre and a displacement of the eye known as exophthalmos in his Thesaurus of the Shah of Khwarazm, the major medical dictionary of its time. Al-Jurjani also established an association between goitre and palpitation. The disease was later named after Irish doctor Robert James Graves, who described a case of goitre with exophthalmos in 1835. The German Karl Adolph von Basedow also independently reported the same constellation of symptoms in 1840, while earlier reports of the disease were also published by the Italians Giuseppe Flajani and Antonio Giuseppe Testa, in 1802 and 1810 respectively, and by the English physician Caleb Hillier Parry (a friend of Edward Jenner) in the late 18th century.
Paracelsus (1493–1541) was the first person to propose a relationship between goitre and minerals (particularly lead) in drinking water. Iodine was later discovered by Bernard Courtois in 1811 from seaweed ash.
Goitre was previously common in many areas that were deficient in iodine in the soil. For example, in the English Midlands, the condition was known as Derbyshire Neck. In the United States, goitre was found in the Great Lakes, Midwest, and Intermountain regions. The condition now is practically absent in affluent nations, where table salt is supplemented with iodine. However, it is still prevalent in India, China, Central Asia, and Central Africa.
Goitre had been prevalent in the alpine countries for a long time. Switzerland reduced the condition by introducing iodised salt in 1922. The Bavarian tracht in the Miesbach and Salzburg regions, which appeared in the 19th century, includes a choker, dubbed Kropfband (struma band) which was used to hide either the goitre or the remnants of goitre surgery.
In the 1920s wearing bottles of iodine around the neck was believed to prevent goitre.
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