What are disorders of the Thyroid Gland?

The thyroid is one of the largest endocrine (hormone producing) glands in the body. This gland is found in the neck below the thyroid cartilage (also known as the Adam's apple in men) and at approximately the same level as the cricoid cartilage. The thyroid controls how quickly the body burns energy, makes proteins, and how sensitive the body should be to other hormones. Hyperthyroidism (overactive thyroid) and hypothyroidism (underactive thyroid) are the most common problems of the thyroid gland.


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How are they caused?

Causes of Hypothyroidism include:

Factors such as iodine deficiency or exposure to Iodine-131 (I-131) can increase the risk of hypothyroidism. There are several other causes of hypothyroidism. Historically, and still in many developing countries, iodine deficiency is the most common cause of hypothyroidism. In iodine-replete individuals, hypothyroidism is mostly caused by Hashimoto's thyroiditis, or by a lack of the thyroid gland or a deficiency of hormones from either the hypothalamus or the pituitary. Hypothyroidism can result from postpartum thyroiditis, a condition that affects about 5% of all women within a year after giving birth. The first phase is typically hyperthyroidism. Then, the thyroid either returns to normal or a woman develops hypothyroidism. Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring life-long treatment. Hypothyroidism can also result from sporadic inheritance, sometimes autosomal recessive.

Causes of Hyperthyroidism include:

Functional thyroid tissue producing an excess of thyroid hormone occurs in a number of clinical conditions. The major causes in humans are:

• Graves' disease (the most common cause with 70-80%)
• Toxic thyroid adenoma
• 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 a number of different kinds of thyroiditis including Hashimoto's (immune mediated), and subacute (DeQuervain's). These may be initially associated 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, as is the rare event of consumption of ground beef contaminated with thyroid tissue, and thus thyroid hormone (termed 'hamburger hyperthyroidism').

• Amiodarone, an anti-arrhythmic drug is structurally similar to thyroxine and may cause both 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 treatment.

What are the symptoms?

Symptoms of Hypothyroidism include:

Early symptoms

• Poor muscle tone (muscle hypotonia)
• Fatigue
• Cold intolerance, increased sensitivity to cold
• Depression
• Muscle cramps and joint pain
• Arthritis
• Goiter
• Thin, brittle fingernails
• Thin, brittle hair
• Paleness
• Dry, itchy skin
• Weight gain and water retention.
• Bradycardia (low heart rate: less than sixty beats per minute)
• Constipation

Late symptoms

• slow speech and a hoarse, breaking voice. Deepening of the voice can also be noticed.
• Dry puffy skin, especially on the face
• Thinning of the outer third of the eyebrows. (Sign of Hertoghe)
• Abnormal menstrual cycles
• Low basal body temperature

Symptoms of Hyperthyroidism include:

Major clinical signs include weight loss (often accompanied by an increased appetite), anxiety, intolerance to heat, fatigue, hair loss, weakness, hyperactivity, irritability, apathy, depression, polyuria, polydipsia, delirium, and sweating. Additionally, patients may present a variety of symptoms such as palpitations and arrhythmias (notably atrial fibrillation), shortness of breath (dyspnea), loss of libido, nausea, vomiting, and diarrhoea. Long term untreated hyperthyroidism can lead to osteoporosis.

In the elderly, these classical symptoms may not be present. Neurological manifestations can include tremours, chorea, myopathy, and in some susceptible individuals (particularly of Asian descent) periodic paralysis. An association between thyroid disease and myasthenia gravis has been recognized. The thyroid disease, in this condition, is autoimmune in nature 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 not well understood. Some very rare neurological manifestations that are dubiously associated with thyrotoxicosis are pseudotumor cerebri, amyotrophic lateral sclerosis and a Guillain-Barré-like syndrome.

Minor eye-related signs, which may be present in any type of hyperthyroidism, are eyelid retraction (stare) and lid-lag.

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.

Neither of these ocular signs should be confused with exophthalmos (protrusion of the eyeball) which occurs specifically and uniquely in Graves' disease. This forward protrusion of the eyes is due to immune mediated inflammation in the retro-orbital (eye socket) fat. Exophthalmos, when present, may exacerbate hyperthyroid lid-lag and stare.

Thyrotoxic crisis is a rare but severe complication of hyperthyroidism, which may occur when a thyrotoxic patient becomes very sick or physically stressed. Its symptoms can include: an increase in body temperature to over 40 degrees Celsius (104 degrees Fahrenheit), tachycardia, arrhythmia, vomiting, diarrhoea, dehydration, coma and death.


How is it diagnosed?


Blood tests

• The measurement of thyroid-stimulating hormone (TSH) levels is often used by doctors as a screening test. Elevated TSH levels can signify an inadequate thyroid hormone production, while suppressed levels can point at excessive unregulated production of hormone.
• If TSH is abnormal, decreased levels of thyroid hormones T4 and T3 may be present; T4 and T3 levels may be determined with blood tests to confirm that their levels are decreased.
• Autoantibodies may be detected in various disease states (anti-TG, anti-TPO, TSH receptor stimulating antibodies).

How is it treated?

Hypothryroidism:
Hypothyroidism is treated with the levorotatory forms of thyroxine (L-T4) and triiodothyronine (L-T3). Both synthetic and animal-derived thyroid tablets are available and can be prescribed for patients in need of additional thyroid hormone. Thyroid hormone is taken daily, and doctors can monitor blood levels to help assure proper dosing. There are several different treatment protocols in thyroid replacement therapy: T4. This treatment involves supplementation of levothyroxine alone, in a synthetic form. It is currently the standard treatment in mainstream medicine. T4 and T3 in Combination: This treatment protocol involves administering both synthetic L-T4 and L-T3 simultaneously in combination.

Temporary medical therapy

Thyrostatics Thyrostatics are drugs that inhibit the production of thyroid hormones, such as carbimazole (used in UK) and methimazole (used in US), and propylthiouracil. Thyrostatics are believed to work by inhibiting the iodination of thyroglobulin by thyroperoxidase, and thus, the formation of tetra-iodothyronine (T4). Propylthiouracil also works outside the thyroid gland, preventing 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. A very high dose is often needed early in treatment, but if too high a dose is used persistently, patients can develop symptoms of hypothyroidism.

Beta-blockers: Many of the common symptoms of hyperthyroidism such as palpitations, trembling, and anxiety are mediated by increases in beta adrenergic receptors on cell surfaces. Beta blockers are a class of drug which offset this effect, reducing rapid pulse associated with the sensation of palpitations, and decreasing tremor and anxiety. This doesn't help the underlying problem of excess thyroid hormone, but makes the symptoms much more manageable, particularly as definitive treatment with thryostatic drugs can take a number of months to work. Propranolol in the UK, and Metoprolol in the US, are most frequently used to augment treatment for hyperthyroid patients.

Permanent treatments

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 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.

Radioiodine In Iodine-131 (Radioiodine):

Radioisotope Therapy, radioactive iodine is given orally (either by pill or liquid) on a one-time basis to destroy the function of a hyperactive gland. Patients who do not respond to the first dose are sometimes given an additional radioactive iodine treatment in a larger dose. The iodine given for ablative treatment is different from the iodine used in a scan. Radioactive iodine is given after a routine iodine scan, and uptake of the iodine is determined to confirm hyperthyroidism. The radioactive 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. Radioactive iodine ablation has been safely used for over 50 years, and the only major reasons for not using it are pregnancy and breast-feeding. A common outcome following radioiodine is a swing to the easily treatable hypothyroidism, and this occurs in 78% of those treated for Graves' thyrotoxicosis and in 40% of those with toxic multinodular goiter or solitary toxic adenoma. Use of higher doses of radioiodine reduces the incidence of treatment failure, with the higher response to treatment consisting mostly of higher rates of hypothyroidism. There is increased sensitivity to radioiodine therapy in thyroids appearing on ultrasound scans as more uniform (hypoechogenic), due to densely packed large cells, with 81% later becoming hypothyroid, compared to just 37% in those with more normal scan appearances (normoechogenic).

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