What is hyperthyroidism? What is the cause? How is it controlled (i.e., prescription medication)? Is it hereditary? hyperthyroidism is an over active thyroid gland. The thyroid gland is located in your neck. A hyperthyroidism patient may have trouble gaining weight as your thyroid gland is run by your pituitary gland and controls virtually everything in your body.
I had/have hypothyroidism which is an under active thyroid gland and some of the symptoms of it was: hands/feet always cold, inability to stand the cold, weight gain, puffy face, tired all the time, lethargic, depressed, no period for months at a time, etc. low thyroid can also cause infertility if left untreated long enough and results in a low metabolism rate (a high metabolism rate in hyperthyroidism patients).
P.S. It is treated with prescription meds. Hypothyroidism patients take synthroid...a synthetic version of the thyroid hormone. On a Question like this you should try to use Google Thyrotoxicosis is the hypermetabolic condition associated with elevated levels of free thyroxine (FT4), free triiodothyronine (FT3), or both. Hyperthyroidism includes diseases that are a subset of thyrotoxicosis (excludes exogenous thyroid hormone intake and subacute thyroiditis) that is caused by excess synthesis and secretion of thyroid hormone by the thyroid. Most clinicians, exclusive of endocrinologists, use the terms hyperthyroidism and thyrotoxicosis interchangeably. This article discusses the causes of thyrotoxicosis associated with hyperthyroidism (excess synthesis and release of thyroid hormone) and surreptitious use of thyroid hormone. Subacute thyroiditis is discussed in the article Thyroiditis, Subacute.
The most common forms of hyperthyroidism include diffuse toxic goiter (Graves disease), toxic multinodular goiter (Plummer disease), and toxic adenoma. Together with subacute thyroiditis, these conditions constitute 85-90% of all causes of thyrotoxicosis.
Pathophysiology
The hypermetabolic effect of thyrotoxicosis affects every organ system. The pituitary gland stimulates the thyroid to make thyroid hormone, which is released into the circulation to reach every cell in the body. Thyroid hormone is necessary for normal growth and development, and it regulates cellular metabolism. Excess thyroid hormone causes an increase in the metabolic rate that is associated with increased total body heat production and cardiovascular activity (increased heart contractility, heart rate, vasodilation).
The most common cause of thyrotoxicosis is Graves disease (50-60%). Graves disease is an organ-specific autoimmune disorder characterized by a variety of circulating antibodies, including common autoimmune antibodies, antithyroperoxidase (anti-TPO), and antithyroglobulin (anti-TG) antibodies. The most important autoantibody is thyroid-stimulating immunoglobulin (TSI). TSI is directed toward epitopes of the thyroid-stimulating hormone (TSH) receptor and acts as a TSH-receptor agonist. Similar to TSH, TSI binds to the TSH receptor on the thyroid follicular cells to activate thyroid hormone synthesis and release and thyroid growth (hypertrophy). This results in the characteristic picture of Graves thyrotoxicosis, with a diffusely enlarged thyroid, very high radioactive iodine uptake, and excessive thyroid hormone levels (see Image 1B) compared to a healthy thyroid (see Image 1A).
Thyroid hormone levels can be extremely elevated in this condition. Clinical findings specific to Graves disease include thyroid ophthalmopathy (periorbital edema, chemosis [conjunctival edema], injection, and proptosis) and, rarely, dermopathy over the lower extremities. This autoimmune condition may be associated with other autoimmune diseases such as pernicious anemia, myasthenia gravis, vitiligo, adrenal insufficiency, and type 1 diabetes mellitus.
The next most common cause of thyrotoxicosis is subacute thyroiditis (approximately 15-20%), a destructive release of preformed thyroid hormone. A typical nuclear scintigraphy scan shows no radioactive iodine uptake in the thyrotoxic phase of the disease. Thyroid hormone levels can be extremely elevated in this condition. This topic is discussed and a typical nuclear scintigraphy scan is shown in the article Subacute Thyroiditis.
Toxic multinodular goiter (Plummer disease) occurs in 15-20% of patients with thyrotoxicosis. It occurs more commonly in elderly individuals, especially in patients with a long-standing goiter. Thyroid hormone excess develops very slowly over time and often is only mildly elevated at the time of diagnosis. As discussed below, very high thyroid hormone levels may occur in this condition after high iodine intake, ie, with contrast or amiodarone exposure. Symptoms of thyrotoxicosis are mild, often because only a slight elevation of thyroid hormone levels is present, and the signs and symptoms of thyrotoxicosis often are blunted (apathetic hyperthyroidism) in older patients. A typical nuclear scintigraphy scan of a toxic multinodular goiter is shown in Image 1C and demonstrates an enlarged thyroid gland with areas of increased and decreased activity.
Toxic adenoma is caused by a single hyperfunctioning follicular thyroid adenoma. Patients with a toxic thyroid adenoma comprise approximately 3-5% of patients who are thyrotoxic. The excess secretion of thyroid hormone occurs from a benign monoclonal tumor that usually is larger than 2.5 cm in diameter. The excess thyroid hormone suppresses TSH levels. Radioactive iodine uptake usually is normal, and the radioactive iodine scan shows only the hot nodule, with the remainder of the normal thyroid gland suppressed because the TSH level is low (see Image 1D).
Several rare causes of thyrotoxicosis exist that deserve mention. Iodide-induced thyrotoxicosis (Jod-Basedow syndrome) occurs in patients with excessive iodine intake, such as after an iodinated radiocontrast study. It occurs in patients with areas of thyroid autonomy such as a multinodular goiter or autonomous nodule. The thyrotoxicosis appears to be a result of loss of the normal adaptation of the thyroid to iodide excess. It is treated by cessation of the excess iodine intake and administration of antithyroid medication. Usually, after depletion of the excess iodine, thyroid functions return to preexposure levels.
Struma ovarii is ectopic thyroid tissue associated with dermoid tumors or ovarian teratomas that can secrete excessive amounts of thyroid hormone and produce thyrotoxicosis.
Metastatic follicular thyroid carcinoma maintains the ability to make thyroid hormone and can cause thyrotoxicosis in patients with bulky tumors.
Patients with a molar hydatidiform pregnancy or choriocarcinoma have extremely high levels of beta human chorionic gonadotropin (bHCG) that can weakly activate the TSH receptor. At very high levels of bHCG, activation of the TSH receptor occurs that is sufficient to cause thyrotoxicosis. Physiological maximum elevation of bHCG at the end of the first trimester of pregnancy is associated with a mirror-image temporary reduction in TSH. Despite the reduction in TSH, the FT4 levels usually remain normal or only slightly above the reference range. As the pregnancy progresses and the bHCG plateaus at a lower level, TSH levels decrease back to normal levels.
History
The presentation of thyrotoxicosis is variable among patients. Thyrotoxicosis leads to an apparent increase in sympathetic nervous system symptoms. Younger patients tend to exhibit symptoms of more sympathetic activation, such as anxiety, hyperactivity, and tremor, while older patients have more cardiovascular symptoms, including dyspnea and atrial fibrillation with unexplained weight loss. The clinical manifestations of thyrotoxicosis do not always correlate with the extent of the biochemical abnormality.
Common symptoms of thyrotoxicosis include the following:
Nervousness
Anxiety
Increased perspiration
Heat intolerance
Tremor
Hyperactivity
Palpitations
Weight loss despite increased appetite
Reduction in menstrual flow or oligomenorrhea (in women)
Common signs of thyrotoxicosis include the following:
Hyperactivity
Tachycardia or atrial arrhythmia
Systolic hypertension
Warm, moist, and smooth skin
Lid lag
Stare
Tremor
Muscle weakness
Generally, a constellation of information, including extent and duration of symptoms, past medical history, social and family history, and physical examination, help guide the clinician to the appropriate diagnosis.
Subclinical hyperthyroidism is associated with no clinical symptoms of thyrotoxicosis. However, certain conditions, such as atrial fibrillation, osteoporosis, or hypercalcemia, may suggest the possibility of thyrotoxicosis. In fact, subclinical hyperthyroidism may be associated with a 3 times increased risk of atrial fibrillation. The prevalence of subclinical hyperthyroidism may be as high as 12% in the general population.
Radiation exposure, whether due to radiation therapy or lower-level x-ray therapy, increases the risk of benign and malignant nodular thyroid diseases, with an observed increase in the incidence of autoimmune hyperthyroidism.
The frequency and severity of symptoms of thyrotoxicosis vary from person to person. Graves disease is an autoimmune disease, and often, a strong family history or past medical history exists with autoimmune diseases such as with rheumatoid arthritis, vitiligo, or pernicious anemia.
The symptoms of Graves disease often are more marked because thyroid hormone levels usually are the highest with this form of hyperthyroidism.
Also consider the diagnosis of Graves disease if any evidence of thyroid eye disease exists, including periorbital edema, diplopia, or proptosis.
Toxic multinodular goiters occur in patients who have had a known nontoxic goiter for many years or decades. Often, patients have emigrated from regions of the world with borderline low-iodine intake or have a strong family history of nontoxic goiter.
Recording a careful family history of autoimmune disease, thyroid disease, and emigration from iodine-deficient areas is important.
Review a complete list of medications. A number of medications contain large amounts of iodine, including expectorants, amiodarone, health food supplements containing seaweed, and iodinated contrast dyes, that can induce thyrotoxicosis in a patient with thyroid autonomy. Rarely, iodine exposure can cause thyrotoxicosis in a patient with an apparently healthy thyroid.
Physical
Physical examination often can help the clinician determine the etiology of thyrotoxicosis.
Thyroid examination: The thyroid is located in the lower anterior neck. The isthmus of the butterfly-shaped gland generally is located just below the cricoid cartilage of the trachea, with the wings of the gland wrapping around the trachea.
Thyrotoxicosis due to Graves disease is associated with a diffusely enlarged and slightly firm thyroid gland. Sometimes, a thyroid bruit is audible using the bell of the stethoscope.
Toxic multinodular goiters occur in goiters that generally are enlarged to at least 2- to 3-times normal size. The gland often is soft, but individual nodules occasionally can be palpated.
A toxic adenoma generally does not cause thyrotoxicosis in a patient until it is at least 2.5 cm in diameter.
If the thyroid is enlarged and painful, the diagnosis is likely subacute painful or granulomatous thyroiditis, but consider degeneration or hemorrhage into a nodule or suppurative thyroiditis.
Thyroid-specific physical examination: Graves thyrotoxicosis can be associated with mild thyroid ophthalmopathy in 50% of patients.
Often, it is manifested only by periorbital edema, but it also can include conjunctival edema (chemosis), injection, poor lid closure, extraocular muscle dysfunction (diplopia), and proptosis.
Evidence of thyroid eye disease and high thyroid hormone levels confirms the diagnosis of autoimmune Graves disease.
Graves disease rarely can affect the skin by deposition of glycosaminoglycans in the dermis of the lower leg. This causes nonpitting edema, usually associated with erythema and thickening of the skin, without pain or pruritus.
Signs of thyrotoxicosis: Usually, signs upon physical examination include sinus tachycardia or atrial fibrillation, systolic hypertension, soft smooth skin, excessive perspiration, palmar erythema and sweating, lid lag, extension tremor, hyperkinesis, and large-muscle weakness hyperthyroidism is when the thyroid is working too much and hypothyroidism is when its not working enough. I think it is usually hereditary. It is controlled by taking prescription medicine. hyperthyroidism occurs when thyroid glands secret too much hormone in your body. type in thyroid problems in yahoo search bar & you will get all the answers you need I did, but I see some people did give you correct answers on your question,it makes me very happy to see smart people on this site, hats off to you all. http://www.webmd.com/hw/thyroid_disorder... (be sure to click next, near the bottom of the page for a lot more information, and also the "Topic Contents, to the right of the description.)
If it is caused by Graves Disease then it is hereditary, otherwise, it could be caused by bacteria or virus or ? .
You may have no symptoms at all. Or:
You may feel nervous, moody, weak, or tired.
Your hands may shake, your heart may beat fast, or you may have problems breathing.
You may be sweaty or have warm, red, itchy skin.
You may have more bowel movements than usual.
You may have fine, soft hair that is falling out.
You may lose weight even though you eat the same or more than usual. I just graduated nursing school in July so I happen to still have my school books and i looked it up for you. Hyperthyroidism is characterized by abnormlly increased synthesis and secretion of thyroid hormones. The most common types are Grave's Disease and multinodular goiter. Grave's disease most often develops in young women. Multinodular goiter occurs most often in women in their sixth and seventh decades. Three methods are used to treat hyperthyroidism:drug therapy, surgery and radiation therapy. Its initially treated with antithyroid drugs such as Tapazole and Lugol's solution.Graves disease is treated surgically by removing most of the thyroid gland. Hyperthyroidism is a condition in which an overactive thyroid gland is producing an excessive amount of thyroid hormones that circulate in the blood.
Some common causes of hyperthyroidism include:
Graves' Disease
Functioning adenoma ("hot nodule") & Toxic Multinodular Goiter (TMNG)
Excessive intake of thyroid hormones
Abnormal secretion of TSH
Thyroiditis (inflammation of the thyroid gland)
Excessive iodine intake Graves' Disease
The options for treating hyperthyroidism include:
Treating the symptoms
Antithyroid drugs
Radioactive iodine
Surgery treating symptoms
One of the main classes of drugs used to treat these symptoms is the beta-blockers (e.g., Inderal, Tenormin, Lopressor).
There are 2 main antithyroid drugs available for use in the United States, methimazole (Tapazole) and propylthiouracil ( PTU)
In the newborn infant: If mother-to-be is taking anti-thyroid medications in leu of hyperthyroidism, it is important to know these medications can be passed on to the unborn child, along with the antibodies that cause hyperthyroidism. It is possible for an abnormal blood test to appear normal due to the anti-thyroid medication crossing the placenta. These medications can mask abnormal results. To ensure the health of your new baby, it is recommended that you have your child rescreened for thyroid disease.
Because this disorder is hereditary, if you have a family history of hyperthyroidism, it is a possibility that your child may acquire this disorder at some time in his/her life. Hyperthyroidism simply means over-secretion of the thyroid hormone from the thyroid gland.It is an imbalance of metabolism caused by overproduction of thyroid hormone.
The thyroid gland is located in the neck. It produces several hormones which control the way that every cell in the body uses energy (metabolism). The thyroid is part of the endocrine system.
Hyperthyroidism or thyrotoxicosis occurs when the thyroid releases too many of its hormones over a short (acute) or long (chronic) period of time. Many diseases and conditions can cause this problem, including:
Graves' disease
Non-cancerous growths of the thyroid gland or pituitary gland, tumors of the testes or ovaries
Inflammation (irritation and swelling) of the thyroid due to viral infections or other causes
Ingestion of excessive amounts of thyroid hormone
Ingestion of excessive iodine
Graves' disease accounts for 85% of all cases of hyperthyroidism. |
