Rabu, 12 November 2008

Thyroid Disorders




1.1. What is the Thyroid?

The thyroid is a small gland, shaped like a butterfly, located in the lower part of your neck. The function of a gland is to secrete hormones. The main hormones released by the thyroid are triiodothyronine, abbreviated as (T3), and thyroxine, abbreviated as (T4). These thyroid hormones deliver energy to cells of the body. It's brownish red, with left and right halves (called lobes) that look like a butterfly's wings. It's light like a butterfly, too, and usually weighs less than an ounce.

As small as it is, though, the thyroid has an enormously important job to do, especially for teens. It manufactures the hormones that help control metabolism and growth. To do its job, the thyroid needs a chemical element called iodine that the body absorbs from the foods you eat and the water you drink. The entire body contains about 50 milligrams of iodine. About 1/5 to 1/3 of that supply (10 to 15 milligrams) is stored in your thyroid. The thyroid combines the iodine with tyrosine (an essential amino acid) to make important hormones. (1.http://www.cancernews.com/data/Article/241.asp)

Thyroid hormones are released from the gland and travel through the bloodstream to your body's cells. They help control the growth and the structure of bones, sexual development (puberty), and many other body functions. By helping your cells convert oxygen and calories into the energy they need to work properly, these hormones are important in determining if your body will mature as it should. Thyroid hormones also directly affect how most of your organs function. So if your thyroid isn't operating properly, you can have problems in lots of other parts of your body.

1.2. Where is the Thyroid and What Does it Do?

Your thyroid is a small bowtie or butterfly-shaped gland, located in your neck, wrapped around the windpipe, behind and below the Adam's Apple area. The thyroid produces several hormones, of which two are key: triiodothyronine (T3) and thyroxine (T4). These hormones help oxygen get into cells, and make your thyroid the master gland of metabolism.

The thyroid has the only cells in the body capable of absorbing iodine. The thyroid takes in iodine, obtained through food, iodized salt, or supplements, and combines it with the amino acid tyrosine. The thyroid then converts the iodine/tyrosine into the hormones T3 and T4. The "3" and the "4" refer to the number of iodine molecules in each thyroid hormone molecule.

When it's in good condition, of all the hormone produced by your thyroid, 80% will be T4 and 20% T3. T3 is considered the biologically more active hormone -- the one that actually functions at the cellular level -- and is also considered several times stronger than T4. Once released by the thyroid, the T3 and T4 travel through the bloodstream. The purpose is to help cells convert oxygen and calories into energy.
As mentioned, the thyroid produces some T3. But the rest of the T3 needed by the body is actually formed from the mostly inactive T4 by a process sometimes referred to as "T4 to T3 conversion." This conversion of T4 to T3 can take place in some organs other than the thyroid, including the hypothalamus, a part of your brain.

The thyroid is part of a huge feedback process. The hypothalamus in the brain releases Thyrotropin-releasing Hormone (TRH). The release of TRH tells the pituitary gland to release Thyroid Stimulating Hormone (TSH). This TSH, circulating in your bloodstream, is what tells the thyroid to make thyroid hormones and release them into your bloodstream.

1.3. What Is Thyroid Disease?

Thyroid disease occurs when the thyroid gland doesn't supply the proper amount of hormones needed by the body. If the thyroid is overactive, it releases too much thyroid hormone into the bloodstream, resulting in hyperthyroidism. ("Hyper" is from the Greek, meaning "over" or "above.") Hyperthyroidism causes the body to use up energy more quickly than it should, and chemical activity (like metabolism) in the cells speeds up. An underactive thyroid produces too little thyroid hormone, resulting in hypothyroidism. ("Hypo" means "under" or "below.") When the amount of hormone released into the bloodstream is below normal, the body uses up energy more slowly, and chemical activity (metabolism) in the cells slows down. Although they are two different conditions, in both hypothyroidism and hyperthyroidism the thyroid can become larger than normal. An enlarged thyroid gland is a lump that can be felt under the skin at the front of the neck. When it is large enough to see easily, it's called a goiter People who don't get enough iodine in their diets also can get an enlarged thyroid, but this is rare in the United States because foods here usually supply enough iodine.

1.4. Causes of Thyroid Disease

What causes thyroid problems? There are a variety of factors that can contribute to the development of thyroid problems:

  1. Shortage of iodine can also trigger some thyroid problems.
  2. Radiation treatment to my head, neck or chest. Radiation treatment for tonsils, adenoids, lymph nodes, thymus gland problems, or acne.
  3. "Nasal Radium Therapy," which took place during the 1940s through 1960s, as a treatment for tonsillitis, colds and other ailments, or as a military submariner and/or pilot who had trouble with drastic changes in pressure.

    Overconsumption of uncooked "goitrogenic" foods, such as brussels sprouts, broccoli, rutabaga, turnips, kohlrabi, radishes, cauliflower, African cassava, millet, babassu, cabbage and kale.

  1. Some drugs, such as lithium and the heart drug cordarone, can cause hypothyroidism.
  2. Radioactive iodine treatment (RAI) for Graves' disease and hyperthyroidism typically leave patients hypothyroid.

    1.5. You have a higher risk of developing thyroid disease if, among a variety of factors

  • You have a family member with a thyroid problem.
  • You or a family member have another autoimmune disease.
  • You're female.
  • You're over 60.
  • You've just had a baby
  • You're near menopause or menopausal.
  • You're a smoker.
  • You've been exposed to radiation.
  • You've been treated with lithium. (2.http://www.thyroid.about.com)



2.1. Thyroid Disorders and Pregnancy

Thyroid disease is present in 2-5 percent of all women and 1-2 percent of women in the reproductive age group. Not unexpectedly, thyroid problems are common in women who are pregnant. In this article we will view pregnancy broadly to include the antepartum (before pregnancy) and postpartum (after pregnancy) periods, as well as pregnancy itself. Both the baby's and mother's well-being are equally important. In this review we will outline our approach to the common thyroid disorders encountered in pregnancy based on questions frequently asked by our own patients.

2.2. Spectrum of Thyroid Disease in Pregnancy

Several of the thyroid disorders which tend to occur during pregnancy are autoimmune in nature. By this we mean that the body develops antibodies directed against thyroid cells, which then affect the way the thyroid gland functions. Antibodies which damage the thyroid cells may result in lymphocytic thyroiditis (inflammation of the thyroid), also known as Hashimoto's disease. These damaging antibodies can reduce the function of the thyroid and lead to hypothyroidism. On the other hand, your body can make antibodies against thyroid tissue which can stimulate thyroid cell function. In this case, hyperthyroidism due to over-function of the thyroid (Graves' disease) may be the result.

2.3. Thyroid Disease and Fertility

Hypothyroidism may be associated with an increased frequency of menstrual periods in patients with mild to moderate thyroid failure, and a lack of menstruation (amenorrhea) when hypothyroidism is severe. There may be problems with ovulation and conception due to the hypothyroidism itself or to associated hormonal changes. For example, in some patients with severe hypothyroidism, the pituitary gland produces increased amounts of a hormone known as prolactin. Increased prolactin secretions can "turn off" normal menstrual cycles. Very rarely, autoimmune ovarian problems coexist with hypothyroidism, with destructive antibodies directed against ovarian tissue. Hyperthyroidism may also be associated with irregular or absent menses, and infertility is common. Thyroid disease should be considered in patients undergoing investigation for menstrual problems or infertility. Fortunately, once treated adequately, neither hypo- nor hyperthyroidism have a major impact on fertility. (3.http://www.thyroid.ca/articles/enge11a.html )

2.4. Planning Pregnancy for Women with Thyroid Disease

2.4.1. Hypothyroidism

One of the most common causes of hypothyroidism is the autoimmune disease called Hashimoto's disease, in which antibodies gradually target the thyroid and destroy its ability to produce thyroid hormone. Symptoms of hypothyroidism usually go along with a slowdown in metabolism, and can include fatigue, weight gain, and depression, among others.

When your thyroid is unable to produce some or all needed thyroid hormone, your thyroid has been surgically removed or treated with radioactive iodine, and you now take thyroid hormone replacement (like levothyroxine), you are considered hypothyroid.

    1. Range hormone (TSH) at your lab

    The TSH test is the most commonly used test for diagnosis and management of hypothyroidism in the United States. But different labs often have slightly different values for what is known as the "TSH reference range." This measure is the range of test values deemed to reflect a normal population.At the lab used by my doctor, the TSH reference range is 0.5 to 5.5 as of fall 2006. A TSH value of less than 0.5 is considered hyperthyroid (overactive thyroid), while a TSH value of more than 5.5 is considered hypothyroid (underactive thyroid). Different labs might use a lower limit of anywhere from 0.35 to 0.6, and an upper threshold of anywhere from 4.0 to 6.0. In any case, it is important for you to be aware of the reference range at the lab where your blood is sent, so you know the standards by which you are being diagnosed. NOTE: Since late 2002, the American Association of Clinical Endocrinologists (AACE) and other professional groups have recommended a narrower TSH reference range of 0.3 to 3.0. This means that hyperthyroidism is now suspected at TSH levels below 0.3, while levels of 3.0 and above are considered potentially indicative of hypothyroidism.

    2. Will you use TSH level as a target

    Some doctors believe that getting a patient into the very top of the normal range is the objective of hypothyroidism treatment. For example, using the 5.5 TSH standard from my own lab, some physicians believe that prescribing thyroid hormone replacement medication to get a patient's TSH down to below 5.5 (even perhaps just down to 5.4) would constitute full treatment. Physicians vary in what TSH level within the normal range they believe makes an ideal target. Some practitioners, for example, might target a TSH level between 1.0 and 2.0 based on their own experience suggesting that patients may feel best at these levels. Other doctors closely follow the new AACE standards discussed earlier, and believe that thyroid hormone replacement treatment should target a TSH level of no more than 3.0 in hypothyroid patients. Finally, some practitioners believe that thyroid treatment decisions should be based primarily on a patient's individual response, with TSH used mainly as a guideline.

    Risk factors for hypothyroidism include:

  • I have a family history of thyroid disease
  • I have had my thyroid "monitored" in the past to watch for changes
  • I had a previous diagnosis of goiters/nodules
  • I currently have a goiter
  • I was treated for hypothyroidism in the past
  • I had post-partum thyroiditis in the past
  • I had a temporary thyroiditis in the past
  • I have another autoimmune disease
  • I have had a baby in the past nine months
  • I have a history of miscarriage
  • I have had part/all of my thyroid removed due to cancer
  • I have had part/all of my thyroid removed due to nodules
  • I have had part/all of my thyroid removed due to Graves' Disease/hyperthyroidism
  • I have had radioactive iodine due to Graves' Disease/hyperthyroidism
  • I have had anti-thyroid drugs due to Graves' Disease/hyperthyroidism

I have the following symptoms of hypothyroidism, as detailed by the Merck Manual, the American Association of Clinical Endocrinologists, and the Thyroid Foundation of America.

  • I am gaining weight inappropriately
  • I'm unable to lose weight with diet/exercise
  • I am constipated, sometimes severely
  • I have hypothermia/low body temperature (I feel cold when others feel hot, I need extra sweaters, etc.)
  • I feel fatigued, exhausted
  • Feeling run down, sluggish, lethargic
  • My hair is coarse and dry, breaking, brittle, falling out
  • My skin is coarse, dry, scaly, and thick
  • I have a hoarse or gravely voice
  • I have puffiness and swelling around the eyes and face
  • I have pains, aches in joints, hands and feet
  • I have developed carpal-tunnel syndrome, or it's getting worse
  • I am having irregular menstrual cycles (longer, or heavier, or more frequent)
  • I am having trouble conceiving a baby
  • I feel depressed
  • I feel restless
  • My moods change easily
  • I have feelings of worthlessness
  • I have difficulty concentrating
  • I have more feelings of sadness
  • I seem to be losing interest in normal daily activities
  • I'm more forgetful lately

I also have the following additional symptoms, which have been reported more frequently in people with hypothyroidism:

  • My hair is falling out
  • I can't seem to remember things
  • I have no sex drive
  • I am getting more frequent infections, that last longer
  • I'm snoring more lately
  • I have/may have sleep apnea
  • I feel shortness of breath and tightness in the chest
  • I feel the need to yawn to get oxygen
  • My eyes feel gritty and dry
  • My eyes feel sensitive to light
  • My eyes get jumpy/tics in eyes, which makes me dizzy/vertigo and have headaches
  • I have strange feelings in neck or throat
  • I have tinnitus (ringing in ears)
  • I get recurrent sinus infections
  • I have vertigo
  • I feel some lightheadedness
  • I have severe menstrual cramps

If you're on thyroid hormone replacement, have a TSH level that's in the normal range, and are still having a range of thyroid-related symptoms, you may be one of the millions of thyroid patients suffering from undertreated hypothyroidism and can benefit from a discussion with your doctor about optimum TSH levels and thyroid drug options. What is undertreated hypothyroidism? It's hypothyroidism at the cellular level that means you still have hypothyroidism symptoms such as fatigue, weight gain, depression, fibromyalgia/muscle and joint aches and pains, hair loss or coarse/dry hair, infertility and more --despite taking thyroid replacement and having a "normal" TSH level. There are two reasons this can occur. First, some doctors believe that providing only enough thyroid hormone to get a patient to mid to high-normal TSH levels is sufficient. And second, the current standard treatment, levothyroxine (brand names include Synthroid, Levoxyl, Levothyroid, Eltroxin, Euthyrox) may not be enough for the majority of people to actually feel well, because the body also needs a small amount of the hormone T3 in addition to the levothyroxine in order to truly feel well. Researchers studying Hashimoto's thyroiditis have found that treatment with the thyroid hormone repalcement drug levothyroxine (LT4) can reduce the incidence of Hashimoto's thyroiditis, as well as help alleviate the symptoms of the disease. In one study of patients who had Hashimoto's disease, but whose TSH thyroid levels were normal ("euthyroid"), one group of patients received levothyroxine treatment, and the other group did not receive treatment.

After 15 months, the treated group had significantly increased Free T4, significantly decreased TSH levels, and a reduction in both anti-thyroglobulin antibody (Tg-Ab) and anti-thyroid peroxidase antibody levels (TPO-Ab). The actual size of the thyroid also decreased in the treated group, while those not receiving treatment had an increase in the size of their thyroid. The researchers reported that although levothyroxine treatment is "mandatory in hypothyroid autoimmune thyroiditis patients, LT4 treatment which is shown to inhibit autoimmune process in animal models is still controversial in euthyroid Hashimoto's disease patients where disease has not destroyed the thyroid gland enough to cause hypothyroidism."

They found, however, that LT4 treatment at doses keeping TSH at low-normal levels appears to be effective not only in decreasing the autoantibody levels but also in the goiter size, which could ultimately prevent progression to overt autoimmune hypothyroidism.

The diagnosis and treatment of hypothyroidism is straightforward. We advise that the adequacy of thyroid hormone replacement therapy be assessed by thyroid function tests, including the thyroid-stimulating hormone (TSH) level, before proceeding with the pregnancy, so as to minimize any possible risk to the mother or her baby that might occur due to hypothyroidism during pregnancy.

2.4.2. Hyperthyroidism

The investigation and management of hyperthyroidism in young women is a bit more complex. With regard to treatment, physicians may recommend either antithyroid medications or radioactive iodine in women of reproductive age. In either case it is essential to control the women's hyperthyroid state before proceeding with pregnancy; this usually takes three to six months. A one-to-two-year course of antithyroid medications, hoping for a remission of thyrotoxicosis, is recommended by some physicians. In the interim, effective birth control measures should be used to prevent pregnancy. The concerns raised by the prospect of continuing to take antithyroid drugs in pregnancy are discussed below. Other physicians prefer to use radioactive iodine to treat women who are contemplating pregnancy, since a complete cure of the of the hyperthyroid condition is assured. Of course, if and when hypothyroidism develops after radioiodine therapy, treatment with thyroid hormone is necessary.

  • What is hyperthyroidism?

    Hyperthyroidism is an overfunctioning of the thyroid gland. This overfunctioning results in the production of too much thyroid hormone. Because the thyroid hormone controls many bodily functions, this increase in the thyroid hormone level causes these bodily functions, such as heartrate, or in some cases blood pressure, to increase, sometimes to very dangerous levels.

  • Causes hyperthyroidism

    Graves' disease, which is an autoimmune disease, toxic nodules or goiters on the thyroid, Excessive thyroid medication given to hypothyroid sufferers, iodine excess, thyroiditis (an inflammation of the thyroid).

  • Graves' Disease described as an autoimmune disorder. What does that mean?

    It means that the disease is caused by a malfunctioning of the immune system of the body - the very system which also protects us from such unpleasant things as bacteria and cancer cells. The immune system works by producing antibodies (also known as immunoglobulins or lymphocytes) which attack and destroy many bad elements in the body, such as virus, bacteria, etc.. The problem is that sometimes this good defense system gets confused and starts attacking good cells. In Grave's Disease, antibodies are produced that attack some of the proteins on the surface of thyroid cells. In response, the thyroid cells produce too much thyroid hormone, which, in turn, overstimulate the thyroid.

  • How common is an autoimmune problem that results in some form of hyperthyroidism?
    This condition is not common. About 10 percent of the population inherits an immune system that can make problems for the thyroid and only one in ten of these will ever have a problem.
  • Just what causes this problem in the immune system to occur?

    It is believed that the environment somehow makes the immune system go haywire. The disease does seem to run in families, but science does not know why. In general, understanding autoimmune diseases is an issue that researchers focusing on extensively.

  • How does the environment make the immune system go wrong?

    The jury is still out on this one. Severe emotional stress is the most commonly suspected culprit, but it is possible for someone to develop the disease without experiencing this stress. Still, reducing stress in life is always a healthy idea. Other factors the can trigger Grave's disease are smoking, radiation to the neck.

  • How can I recognize Graves' Disease?

    Even if you have Graves' disease, it can take weeks, or even months, before you suspect you are sick because the symptoms build very gradually. You may think you are just experiencing stress, or feeling extra anxious. Or the disease may actually make you happy in the short term, as one of the side effects of speeding up the thyroid can be weight loss. However, in the longer term, less desirable symptoms, such as muscle weakness, insomnia and trembling can also result. The pulse will likely increase, along with an inability to tolerate heat and abnormally high sweating. You may experience hair loss and diarrhea is common. Women may find that the menstrual flow will lighten and the time between periods grow longer. Depression can also enter the picture. And, as mentioned above, blood pressure and heart rate can increase to dangerous levels. But Graves' Disease often has the most visible impact on the skin and eyes.

  • How does Graves' Disease affect the eyes?

    Graves' disease is associated with inflammation of the eyes, swelling of the tissues around the eyes, and bulging of the eyes. However, 99% of the time, this inflammation will not cause serious or permanent trouble. Early signs of Grave's Disease affecting the eyes include: bulging of the eyes due to inflammation of the tissues behind the eyeball (the medical term is exophthalmos), blurred or diminished vision, red or inflamed eyes, double vision.

    It is believed that the swelling is caused by antibodies attacking the tissues of the eye muscles. There may also be a sensitivity to light, and a continual feeling that there is something in the eyes. Such symptoms usually appear within six months of when the diagnosis of Graves' Disease is made.

  • How does Graves' Disease affect the skin?

    Although it is rare, Graves' Disease patients will sometimes get a lumpy reddish thickening of the skin in front of the shins (pretibial skin). This condition is known as "pretibial myxedema" (also more generically referred to as dermopathy). It's usually painless, not serious and, may not start even when the hyperthyroidism starts. As with the eyes, it is believed that this swelling in the pretibial skin is caused by antibodies attacking these tissues. What else do I need to know about Graves' Disease?

      - Where hyperthyroidism eye complications occur.

      - Smoking tends to worsen the eye problems associated with Graves' disease, yet another reason to quit.

      - It is more prevalent in women than in men, by a ratio of about 8 to 1.

      - Typically occurs in middle age.

    Now that you know something about hyperthyroidism, the dangers, the causes, and it's most common forms, in the next part of the series, we'll look at how hyperthyroidism is diagnosed.

  • Diagnosis one of the variations of hyperthyroidism?

    Initial diagnosis usually simply requires a physical examination for the following:

      - Enlarged thyroid gland

      - Rapid heart beat (tachycardia) or heart palpitations

      - Smooth, velvety skin

      - Tremor of the fingertips

      - For Graves' disease, eyes and skin

Other symptoms are:

      - Fatigue

      - Sweaty palms

      - Weight loss

      - Fine brittle hair

      - Restlessness

      - Depression

      - Increased appetite

      - Changes in sex drive

      - Muscle weakness, especially in the upper arms and thighs

      - Shortened attention span

      - Heat intolerance

      - Increased sweating

      - Nervousness and irritability

      - Restless sleep or insomnia

      - Erratic behavior

      - For women, irregular menstrual cycle and reduced menstrual flow

      - Infertility, recurrent miscarriage

      - Increased frequency of bowel movements

    A family medical history may also hold clues to a diagnosis of hyperthyroidism, specifically if a family member:

    - Had either or an underactive thyroid

    - Had hair that went gray starting in their 20's

    - Had problems with their immune system, such as juvenile diabetes

    A final diagnosis is always made by means of a common blood test which will expose abnormally high thyroid hormone levels and low levels of the thyroid-stimulating hormone (TSH) produced by the pituitary gland. Low blood TSH levels are the most reliable test of most hyperthyroidism. In rare cases, the pituitary gland produces excess amounts of TSH. Then there will be increased levels of both the TSH and thyroid hormones in the blood. Sometimes, additionally, the thyroid-stimulating antibodies (TSAb) or Thyroid Stimulating Immunoglobulin (TSI) in the blood will also be measured. And finally, a radioactive picture of the thyroid, made by ingesting radioactive iodine (known as RAI) in the mouth, may also be taken to see if the thyroid gland is overactive.

  • Can excessive thyroid medication given to hypothyroid sufferers cause hyperthyroidism?
    In fact, the dosages prescribed may sometimes be so strong that they cause the thyroid to become hyperthyroid. In such a case, your doctor should reduce the dosage of your medication until the thyroid hormone in your system is back at normal levels.
  • What about iodine as a cause of hyperthyroidism?

    Iodine is used by the thyroid gland to make thyroid hormones. Too much iodine can result in hyperthyroidism. Hyperthyroidism caused by an excess of iodine is usually characterized by an abnormal thyroid gland - as in a gland with goiters or a multinodular goiter. Iodine excess can be caused by certain medications that contain larger amounts on iodine. An example is amiodarone - a heart medicine.

  • Is there any way to quickly control the dangerous symptoms of hyperthyroidism?
    Regardless of the method of treatment eventually used, a doctor may initially recommend a beta-adrenergic blocking drug - also known as beta blockers - such as atenolol (Tenormin ), nadolol (Corgard ), metoprolol (Lopressor ), or propranolol (Inderal ) to block the action of circulating thyroid hormone on your body tissues, slow your heart rate and reduce your nervousness. These drugs can be useful in rapidly reducing these potentially dangerous symptoms until your treatment has taken effect. However, they should not be used if you have asthma or heart failure, as they can worsen these conditions. Diabetic patients taking insulin should also take care because the beta-blocking drugs may mask the warning symptoms of low blood sugar. Finally, these drugs are not a substitute for treatment, but they will normally make you feel better - sometimes in as little as a few hours.
  • What is the initial treatment for Graves' Disease?

    The first course of action - when the disease is mild, or occurs in children or young adults, or needs to be promptly controlled (as with elderly patients whose heart disease puts them at risk from the increased heart rate associated with Grave's Disease) - is a course of antithyroid drugs, such as propylthiouracil (PTU) and methimazole (Tapazole ). These drugs make it more difficult for your thyroid to use the iodine it needs to make the thyroid hormone, resulting in a decrease in thyroid hormone production. Although both drugs can be used during pregnancy, PTU is preferable. In about 5% of cases, a skin rash will result. In about 0.05% of cases, patients will develop a low white count, thereby increasing the risk of serious infection.

  • Are there any side effects to antithyroid drugs?

    In about 5% of cases, antithyroid drugs cause allergic reactions such as skin rashes, hives, and sometimes fever and joint pains. A much more serious potential side effect is a decrease in the white blood cells that are a part of the immune system - thereby resulting in a decrease in your resistance to infection. In very rare cases, these cells may disappear entirely (a condition called agranulocytosis) - which can be potentially fatal if there is a serious infection. If, while taking these drugs, you experience an infection, stop taking the drug immediately and get a white blood count that same day. If the white count has been lowered and you continue taking the drug, the infection could become fatal. However, a lowered white count will return to normal once you have stopped taking the drug. Hypothyroidism can result from the use of antithyroid drugs, although it is far less likely to result from this treatment than from surgery or radiation.

  • If the drugs don't work, what is the next treatment option?

    Most hyperthyroid patients wind up being, treated with radioactive iodine otherwise known as RAI. This RAI is administered by mouth, by means of a capsule or a liquid. What happens then is that the RAI goes from the stomach into the bloodstream and eventually into the thyroid gland.

  • What happens to this radiation in my body?

    Eventually, the body will pass much of the RAI out through urine. Any remaining RAI will become nonradioactive.

  • Then just how safe is this radiation treatment?

    This treatment has been used since 1940, and no serious complications from RAI treatment have become apparent over nearly 50 years of use. However, RAI should not be taken during pregnancy or breast feeding.

  • How fast does RAI work?

    Most patients get relief in three to six months. However, if the initial dose was too small, it may need to be repeated.

  • Are there any side effects to the radiation?

    The main side effect is, that because the damage to the thyroid cannot be controlled, the thyroid of most patients becomes underactive (hypothyroidism) after RAI. This condition is then treated with a thyroid hormone supplement. This may seem silly - trading one thyroid problem for another. But hyperthyroidism is much more dangerous, and difficult to control, than is hypothyroidism. So while becoming hypothyroid may not be a perfect outcome, it is much better than being hyperthyroid.

  • Are there any alternatives to the drugs or radiation?

    Surgery to remove all or part of the thyroid gland (known as a thyroidectomy) will permanently cure hyperthyroidism. However, several things need to happen before surgery takes place.

      1. First, surgery can be risky unless the hyperthyroidism is already being controlled by an antithyroid or a beta blocking drug, described below. Therefore, you will take either propylthiouracil or Tapazole to lower your thyroid hormone levels. You should reach normal levels in about six weeks

      2. Often, for several days prior to surgery, you will also take some drops of nonradioactive iodine (either Lugol's iodine or supersaturated potassium iodide). This has the effect of reducing the blood supply to the thyroid gland, thereby making surgery easier and safer.

    The goal of the surgery is to remove just enough of the gland so that thyroid production is back to normal. As with many things medical, determining how much of the gland to take is part science and part art. If too much is taken, than the patient can become hypothyroid. There can also be other complications resulting from the surgery. One is vocal cord paralysis. Another, is accidental removal of the parathyroid glands, which are located in the neck in back of the thyroid gland. Because the parathyroid glands regulate the amount of calcium in the body, their removal will result in low calcium levels.

      Surgery is now reserved for special cases, including:

    - pregnant women who cannot tolerate antithyroid medication

    - people who do not want RAI but do want a permanent form of treatment

2.4.3. Risk and Factor Diagnosis

My risk factors for hyperthyroidism include:

  • I have a family history of thyroid disease
  • Parent (type of thyroid problem)
  • Grandparent (type of thyroid problem)
  • Sibling (type of thyroid problem)
  • Child (type of thyroid problem)

I have had my thyroid "monitored" in the past to watch for changes

  • I had a previous diagnosis of goiters/nodules
  • I currently have a goiter/enlargement in my thyroid and/or thyroid nodules
  • I was treated for hypothyroidism or hyperthyroidism in the past
  • I had post-partum thyroiditis or hyperthyroidism during pregnancy in the past
  • I had a temporary thyroiditis in the past
  • I have another autoimmune disease
  • I am pregnant now, or I have had a baby in the past nine months
  • I have a history of miscarriage
  • I have had radioactive iodine in the past due to Graves' Disease/hyperthyroidism
  • I have taken anti-thyroid drugs in the past due to Graves' Disease or a diagnosis of hyperthyroidism

Symptoms of hyperthyroidism, as detailed by the Merck Manual, the American Association of Clinical Endocrinologists, and the Thyroid Foundation of America.

  • My heart feels like it's skipping a beat, racing and I feel like I'm having heart palpitations.
  • My pulse is unusually fast
  • My pulse, even when resting or in bed, is high
  • My hands are shaking, I'm having hand tremors
  • I feel hot when others feel cold, I am feeling inappropriately hot or overheated
  • I'm having increased perspiration
  • I am losing weight inappropriately
  • I am losing weight but my appetite has increased
  • I feel like I have a lot of nervous energy that I need to burn off
  • I am having diarrhea or loose or more frequent bowel movements
  • I feel nervous or irritable
  • My skin looks or feels thinner
  • My muscles feel weak, particularly the upper arms and thighs
  • I am having difficulty getting to sleep, staying asleep, or going back to sleep after awakening in the middle of the night
  • I feel fatigued, exhausted
  • My hair is coarse and dry, breaking, brittle, falling out
  • My skin is coarse, dry, scaly, thin
  • I have a hoarse or gravely voice
  • I have pains, aches in joints, hands and feet
  • I am having irregular menstrual cycles (shorter, longer, or heavier, or more frequent, or not at all)
  • I am having trouble conceiving a baby
  • I have had one or more miscarriages
  • I feel depressed
  • I feel restless, or anxious
  • I have had panic attacks.
  • I've recently been diagnosed as having panic disorder, anxiety disorder, or panic attacks
  • I have puffiness and swelling around the eyes and face
  • My eyes seem to be enlarging, or getting more "bug-eyed" looking
  • My moods change easily
  • I have feelings of worthlessness
  • I have difficulty concentrating or focusing
  • I have more feelings of sadness
  • I seem to be losing interest in normal daily activities
  • I'm more forgetful lately

I also have the following additional symptoms, which have been reported more frequently in people with hyperthyroidism:

  • My hair is falling out
  • I can't seem to remember things
  • I have no sex drive, or am having sexual performance problems
  • I am getting more frequent infections, that last longer
  • I feel shortness of breath and tightness in the chest
  • My eyes feel gritty and dry
  • My eyes feel sensitive to light
  • My eyes get jumpy/tics in eyes, which makes me dizzy/vertigo and have headaches
  • I have strange feelings in neck or throat
  • I have tinnitus (ringing in ears)
  • I get recurrent sinus infections
  • I have vertigo
  • I feel some lightheadedness
  • I have severe menstrual cramps (4.http://www.thyroid.about.com)

2.4.4. Thyroid Disease in the Mother During Pregnancy Thyroid Function in Pregnancy

Thyroid gland function is normal in pregnancy, although normal pregnant women often develop symptoms and signs suggesting hyperthyroidism, such as rapid heat beat or palpitations, sweating, and heat intolerance. The metabolic rate is also increased in pregnancy, so it is easy to see why hyperthyroidism is often suspected even though it is actually present in only one out of 1,000 pregnancies. The normal thyroid gland may be slightly larger in pregnancy, but the presence of even a modestly enlarged gland usually means that there is an underlying thyroid problem which requires investigation. The total serum thyroxine (T4) and triiodothyronine (T3) levels are increased in pregnancy due to high levels of estrogen which, in turn, increase the thyroid hormone-binding protein concentrations. Although this makes thyroid functions more difficult to interpret, thyroid hormone production is normal in pregnant women.

The baby's thyroid begins to function after ten to twelve weeks of pregnancy. Thyroid hormones are important for development of the fetal nervous system and these are probably derived from both the baby's thyroid gland secretion as well as small amounts of the mother's thyroid hormone that cross the placenta. Iodine in the mother's diet readily crosses the placenta and is used by the fetal thyroid gland to make thyroid hormone. Iodine deficiency can cause newborn hypothyroidism or mental retardation (cretinism) and is a major world health problem in underdeveloped countries. Since there is an overabundance of iodine in the American diet, disorders caused by a lack of dietary iodine do not occur here. What are the normal changes in thyroid function associated with pregnancy?

Hormone Changes. A normal pregnancy results in a number of important physiological and hormonal changes that alter thyroid function. These changes mean that laboratory tests of thyroid function must be interpreted with caution during pregnancy. Thyroid function tests change during pregnancy due to the influence of two main hormones: human chorionic gonadotropin (hCG), the hormone that is measured in the pregnancy test and estrogen, the main female hormone. HCG can weakly turn on the thyroid and the high circulating hCG levels in the first trimester may result in a slightly low TSH. When this occurs, the TSH will be slightly decreased in the first trimester and then return to normal throughout the duration of pregnancy (see Table 1).


1st Trimester 2nd Trimester 3rd Trimester

TSH .................................Normal or Decreased ............ Normal ......................Normal

Free T4 ...................................... Normal........................ Normal ......................Normal

Free T3 .......................................Normal........................ Normal ......................Normal

Total T4 ......................................... High .......................... High ......................... High

Total T3 ......................................... High .......................... High ......................... High

T3 Resin Uptake ............................ Low .......................... Low .......................... Low

(Inverse measure of protein binding)

Free T4 Index (FT4I, FTI) ..........Normal....................... Normal ......................Normal

Estrogen increases the amount of thyroid hormone binding proteins in the serum which increases the total thyroid hormone levels in the blood since >99% of the thyroid hormones in the blood are bound to these proteins. However, measurements of “Free” hormone (that not bound to protein, representing the active form of the hormone) usually remain normal. The thyroid is functioning normally if the TSH, Free T4 and Free T3 are all normal throughout pregnancy. Size Changes. The thyroid gland can increase in size during pregnancy (enlarged thyroid = goiter). However, pregnancy-associated goiters occur much more frequently in iodine-deficient areas of the world. It is relatively uncommon in the United States, which is thought to be relatively iodine-sufficient. If very sensitive imaging techniques (ultrasound) are used, it is possible to detect an increase in thyroid volume in some women. This is usually only a 10-15% increase in size and is not typically apparent on physical examination by the physician. However, sometimes a significant goiter may develop and prompt the doctor to measure tests of thyroid function. Function thyroid of the mother and the baby

For the first 10-12 weeks of pregnancy, the baby is completely dependent on the mother for the production of thyroid hormone. By the end of the first trimester, the baby’s thyroid begins to produce thyroid hormone on its own. The baby, however, remains dependent on the mother for ingestion of adequate amounts of iodine, which is essential to make the thyroid hormones. The World Health Organization recommends iodine intake of 200 micrograms/day during pregnancy to maintain adequate thyroid hormone production. The normal diet in the United States contains sufficient iodine so additional iodine supplementation is rarely necessary. Causes of hyperthyroidism during pregnancy

Overall, the most common cause (80-85%) of maternal hyperthyroidism during pregnancy is Graves’ disease and occurs in 1 in 1500 pregnant patients. In addition to other usual causes of hyperthyroidism, very high levels of hCG, seen in severe forms of morning sickness (hyperemesis gravidarum), may cause transient hyperthyroidism. The diagnosis of hyperthyroidism can be somewhat difficult during pregnancy, as 123I thyroid scanning is contraindicated during pregnancy due to the small amount of radioactivity, which can be concentrated by the baby’s thyroid. Consequently, diagnosis is based on a careful history, physical exam and laboratory testing. Risks Graves’ Disease/hyperthyroidism to the mother

Graves’ disease may present initially during the first trimester or may be exacerbated during this time in a woman known to have the disorder. In addition to the classic symptoms associated with hyperthyroidism, inadequately treated maternal hyperthyroidism can result in early labor and a serious complication known as pre-eclampsia. Additionally, women with active Graves’ disease during pregnancy are at higher risk of developing very severe hyperthyroidism known as thyroid storm. Graves’ disease often improves during the third trimester of pregnancy and may worsen during the post partum period. Risks Graves’ Disease/hyperthyroidism to the baby

The risks to the baby from Graves’ disease are due to one of three possible mechanisms:

    1. Uncontrolled maternal hyperthyroidism: Uncontrolled maternal hyperthyroidism has been associated with fetal tachycardia (fast heart rate), small for gestational age babies, prematurity, stillbirths and possibly congenital malformations. This is another reason why it is important to treat hyperthyroidism in the mother.

    2. Extremely high levels of thyroid stimulating immunogloblulins (TSI): Graves’ disease is an autoimmune disorder caused by the production of antibodies that stimulate thyroid gland referred to as thyroid stimulating immunoglobulins (TSI). These antibodies do cross the placenta and can interact with the baby’s thyroid. Although uncommon (2-5% of cases of Graves’ disease in pregnancy), high levels of maternal TSI’s, have been known to cause fetal or neonatal hyperthyroidism. Fortunately, this typically only occurs when the mother’s TSI levels are very high (many times above normal). Measuring TSI in the mother with Graves’ disease is often done in the third trimester. In the mother with Graves’ disease requiring antithyroid drug therapy, fetal hyperthyroidism due to the mother’s TSI is rare, since the antithyroid drugs also cross the placenta. Of potentially more concern to the baby is the mother with prior treatment for Graves’ disease (for example radioactive iodine or surgery) who no longer requires antithyroid drugs. It is very important to tell you doctor if you have been treated for Graves’ Disease in the past so proper monitioring can be done to ensure the baby remains healthy during the pregnancy.

    3. Anti-thyroid drug therapy (ATD). Methimazole (Tapazole) or propylthiouracil (PTU) are the ATDs available in the United States for the treatment of hyperthyroidism. Both of these drugs cross the placenta and can potentially impair the baby’s thyroid function and cause fetal goiter. Historically, PTU has been the drug of choice for treatment of maternal hyperthyroidism, possibly because transplacental passage may be less than with Tapazole. However, recent studies suggest that both drugs are safe to use during pregnancy. It is recommended that the lowest possible dose of ATD be used to control maternal hyperthyroidism to minimize the development of hypothyroidism in the baby or neonate. Neither drug appears to increase the general risk of birth defects. Overall, the benefits to the baby of treating a mother with hyperthyroidism during pregnancy outweigh the risks if therapy is carefully monitored.

2.4.5. Risks hypothyroidism to the mother

Untreated, or inadequately treated, hypothyroidism has been associated with maternal anemia (low red blood cell count), myopathy (muscle pain, weakness), congestive heart failure, pre-eclampsia, placental abnormalities, low birth weight infants, and postpartum hemorrhage (bleeding). These complications are more likely to occur in women with severe hypothyroidism. Most women with mild hypothyroidism may have no symptoms or attribute symptoms they may have as due to the pregnancy.

2.4.6. Risks of maternal hypothyroidism to the baby

Thyroid hormone is critical for brain development in the baby. Children born with congenital hypothyroidism (no thyroid function at birth) can have severe cognitive, neurological and developmental abnormalities if the condition is not recognized and treated promptly. These developmental abnormalities can largely be prevented if the disease is recognized and treated immediately after birth. Consequently, all newborn babies in the United States are screened for congenital hypothyroidism so they can be treated with thyroid hormone replacement therapy as soon as possible. The effect of maternal hypothyroidism on the baby’s brain development is not as clear. Untreated severe hypothyroidism in the mother can lead to impaired brain development in the baby. This is mainly seen when the maternal hypothoidism is due to iodine deficiency, which also affects the baby However, recent studies have suggested that mild brain developmental abnormalities may be present in children born to women who had mild untreated hypothyroidism during pregnancy. At this time there is no general consensus of opinion regarding screening all women for hypothyroidism during pregnancy. However, some physician groups recommend checking a woman’s TSH value either before becoming prenant (pre-pregnancy counseling) or as soon as pregnancy is confirmed. This is especially true in women at high risk for thyroid disease, such as those with prior treatment for hyperthyroidism, a positive family history of thyroid disease and those with a goiter. Clearly, woman with established hypothyroidism should

have a TSH test once pregnancy is confirmed, as thyroid hormone requirements increase during pregnancy, often leading to the need to increase the levothyroxine dose. If the TSH is normal, no further monitoring is typically required. This issue should be discussed further with your health care provider, particularly if you are contemplating

pregnancy. Once hypothyroidism has been detected, the woman should be treated with levothyroxine to normalize her TSH and Free T4 values.

2.4.7. How should a woman with hypothyroidism be treated during pregnancy?

The treatment of hypothyroidism in a pregnant woman is the same as for a man or non-pregnant woman, namely, adequate replacement of thyroid hormone in the form of synthetic levothyroxine. It is important to note that levothyroxine requirements frequently increase during pregnancy, often times by 25 to 50 percent. Occasionally, the levothyroxine dose may double. Ideally, hypothyroid women should have their levothyroxine dose optimized prior to becoming pregnant. Women with known hypothyroidism should have their thyroid function tested as soon as pregnancy is detected and their dose adjusted by their physician as needed to maintain a TSH in the normal range. Thyroid function tests should be checked approximately every 6-8 weeks during pregnancy to ensure that the woman has normal thyroid function throughout pregnancy. If a change in levothyroxine dose is required, thyroid tests should be measured 4 weeks later. As soon as delivery of the child occurs, the woman may go back to her usual pre-pregnancy dose of levothyroxine. It is also important to recognize that prenatal vitamins contain iron that can impair the absorption of thyroid hormone from the gastrointestinal tract. Consequently, levothyroxine and prenatal vitamins should not be taken at the same time and should be separated by at least 2-3 hrs. (5.http://www.thyroid.org/patients/brochures/Thyroid_Dis_Pregnancy_broch.pdf)

2.5. Thyrotoxicosis

Thyrotoxicosis means an excess of thyroid hormone in the body. Having this condition also means that you have a low level of thyroid stimulating hormone, TSH, in your bloodstream, because the pituitary gland senses that you have “enough” thyroid hormone. If you are thyrotoxic, you may feel nervous or irritable, because all of your body’s functions are speeding up.

Hyperthyroidism, also referred to as an overactive thyroid is the most common cause of thyrotoxicosis and, occurs when your thyroid gland produces too much thyroid hormone. The most common cause of hyperthyroidism is Graves' Disease, in which the immune system, for reasons that are not clearly understood, releases antibodies that attack or “bind” to thyroid cells. The process stimulates the thyroid gland, causing it to grow and produce high levels of thyroid hormone. As many as 70-80% of patients with hyperthyroidism have Graves’ disease and it may run in families.

Graves' Disease is also referred to as diffuse toxic goiter because it affects the entire thyroid gland (diffuse), causes people with the condition to appear flushed (toxic) and the gland becomes enlarged (goiter). People who have an autoimmune disease, such as Graves’ disease, are at higher risk of developing other autoimmune diseases, such as type 1 diabetes or Addison’s disease. A single nodule or multiple nodules in the thyroid gland which can produce excessive thyroid hormone also can cause hyperthyroidism.

Thyrotoxicosis can also come from inflammation of the gland (thyroiditis ) or from taking too much thyroid medication. In these cases the thyroid gland itself is not overactive, but there is still too much thyroid hormone in the blood. Untreated, thyrotoxicosis can lead to serious medical complications such as heart rhythm disturbances and Osteoporosis, caused from the long-term effects of hormone overproduction.

Another condition, called subclinical hyperthyroidism, may be diagnosed when you have low levels of thyroid stimulating hormone (TSH) but normal levels of thyroid hormone. Your doctor may treat asymptomatic (without symptoms) subclinical hyperthyroidism to avoid future symptoms.

2.5.1. Signs and Symptoms

Mild thyrotoxicosis may not cause any symptoms to begin with. Symptoms associated with more severe cases include:

  • Nervousness
  • Irritability
  • Fatigue
  • Fast heartbeat
  • Weight loss
  • Insomnia
  • Hair loss
  • Thin skin
  • Intolerance to heat
  • Increased perspiration
  • Muscle aches
  • Weakness in upper arms and thighs
  • Increased bowel movements
  • Decreased menstrual flow
  • Eye irritation or inflammation; “bulging” eyes

2.5.2. Treatment

Treatment for thyrotoxicosis will depend upon your age, the cause and severity of your illness, and other medical conditions you may have. Untreated thyrotoxicosis can lead to serious medical complications such as heart rhythm disturbances and osteoporosis caused from the long-term effects of hormone overproduction.

  • Drug treatment

    Two “antithyroid” drugs are available to treat hyperthyroidism. These drugs inhibit the thyroid gland’s production of thyroid hormone. Drugs used for this purpose include methimazole (Tapazole) and propylthiouracil (PTU).

    Another class of drugs called beta adrenergic blocking agents can diminish some of the symptoms of thyrotoxicosis. The level of thyroid hormone in your blood, however, is not affected, so you will continue to have high levels of this hormone circulating in your bloodstream. These drugs include propranolol (Inderal), atenolol (Tenormin), metoprolol (Lopressor) and nadolol (Corgard). They are usually used in combination with other treatment for thyrotoxicosis.

  • Radioactive iodine

    Choose to treat your condition by permanently damaging the cells in the thyroid that produce thyroid hormone. This can be accomplished with the use of radioactive iodine, which has been utilized as a treatment regimen since the 1940s. Radioactive iodine is a tasteless and odorless substance that is swallowed in capsule or liquid form. Once ingested, it is absorbed into the bloodstream and is taken up by the overactive thyroid cells. Over a period of several weeks your thyroid gland will shrink in size and blood levels of thyroid hormone and thyroid stimulating hormone (TSH) will return to normal. A second radioactive iodine treatment may be needed to achieve desired results. Most patients who have had radioactive iodine therapy eventually become hypothyroid because their thyroid gland is not producing enough thyroid hormone. This condition is treated with daily intake of thyroid hormone replacement therapy.

  • Surgery
    Recommend that you have surgery to remove all or part of your thyroid gland. You may be a candidate for partial removal of your thyroid gland if one or more nodules on the gland are overactive. However, if many nodules are involved or if your entire thyroid gland is overactive, your doctor may suggest that most or all of it be removed. The upside to this type of treatment is that your hyperthyroid condition – and the severe complications that can arise from it – will be greatly reduced. Surgery for hyperthyroidism is indicated in only a limited number of patients. Your doctor will talk to you about the pros and cons of this treatment and whether or not it is the best option for you. Surgery to remove part or all of your thyroid gland is done under a general anesthetic in the operating room. Your doctor will make a thin incision along the front of your neck, usually along a natural crease in your skin. He/she will then remove the affected part of your gland. Surgery to remove one lobe of your thyroid is called a lobectomy. Sometimes the central portion (isthmus) that connects the two lobes is also removed (isthmusectomy). Surgery to remove most of your gland is called a subtotal thyroidectomy. Surgery to remove your entire gland is called a total thyroidectomy. In some instances, your doctor will determine how much of the gland to remove during surgery. The total time for your operation is about 1 ½ hours. You may experience a sore throat and hoarseness for several weeks after your operation, which is normal with this type of surgery. Once the majority of your gland is removed, you will need to take thyroid hormone replacement therapy every day to replace the hormone that is not being made naturally in your body. Your doctor will also talk to you about regular check-ups and blood tests to help monitor your condition. (6.https://www.virginiamason.org/home/body.cfm?id=589)



In dealing with thyroid disease in pregnancy, the physician and patient should be aware of problems that occur before and after, as well as during the actual pregnancy. There should be equal concern for the welfare of both the mother and baby. Fortunately, most thyroid conditions can be recognized, problems can be anticipated, and effective treatment is available. The outcome is almost always a healthy one, for both the mother and her baby.

The first thing you should know about finding a thyroid specialist is that you may not need one after all. If your problem is hypothyroidism that has been diagnosed, your physician may choose to start you on thyroid hormone and observe the results. If your symptoms disappear and you feel well again, periodic rechecking of your serum TSH level to be sure the dose is right may be all that's necessary. On the other hand, most patients with Graves' disease or cancer should see a thyroid specialist. And your physician is likely to be the best person to find a thyroid specialist for you in your area. TFA has the names of thyroid specialists all over the country, chosen for referral because they are members of the American Association of Clinical Endocrinologists, the American Thyroid Association, or The Endocrine Society, which are the three large professional organizations of these specialists in the United States and Canada.

You may have an overactive thyroid that has not responded to medical treatment and there may be reasons for not taking treatment with radioactive iodine. You may have a very large thyroid, or goiter, that is disfiguring or interfering with breathing or swallowing. You may have a nodule, and your physician wants a biopsy to tell if it contains cancer. You may have a thyroid tumor that needs to be removed, or a recurrence of a previous cancer.

Several types of surgeons operate on the thyroid, including general surgeons, otolaryngologists (ear, nose, and throat specialists), cancer surgeons, thoracic (chest) surgeons, and even surgeons who specialize in operating on patients with endocrine problems. On the other hand, your problem could be Graves' disease and you may need eye surgery. Here an ophthalmologist or plastic surgeon may be the best choice. Any one of these could be right for your problem.

The most important considerations for you and your physician are the type and extent of your problem and the skill and experience of the particular surgeon with that disorder. Here are some questions to ask. Has the surgeon had good results with your type of problem? Does the doctor have special training in endocrine operations or neck surgery? How often does he or she do this type of operation? Does the surgeon have special credentials such as board certification, or membership in the American Association of Endocrine Surgeons? What is the surgeon's complication rate for problems such as injury to the laryngeal nerve which supplies the vocal cords or to the parathyroid glands?

There is another way to look at this too. In this era of "managed" health care, health insurance companies are taking an increasingly active role in deciding who should perform surgery of many types. But in your special circumstance of thyroid surgery, which can be unexpectedly delicate and complicated, not everyone who does thyroid operations will be right for you. Make sure that the choice of the surgeon is matched to the operation which is to be performed.



  1. Adler, R. & M. Hayes 1990. Psychosocial Factors in Pregnancy and The Experience of Labor: A Prospective Study. Journal of Psychosomatic Obstetrics Gynaecology 11 1990. Hal 47-55. New Jersey: The Partenon Publishing Group.
  2. Bardwick, Yudith, M. 1971. Psychology of Women A Study of Biocultural Conflicts. New York: Harper & Row Publishers.
  3. Cameron, JL; Current Surgical Therapy. 7th ed. Mosby Year Book, Inc.; July 2000.
  4. Chabon, SL; “Identification and evaluation of thyroid nodules.” Lippincott’s Primary Care Practice Nov-Dec 1997; 1(5): 499-504.
  5. Daniels, GH; “Thyroid nodules and nodular thyroids: a clinical review.” Comprehensive Therapy April 1996; 22(4): 239-250.
  6. Davids, A. (Ed.) 1961. Anxiety, Pregnancy, Chilbirth Abnormalities. Journal of Consulting Psychology 25. Hal. 74-75.

    Malinowski, Bronislaw. 1927. Sex and Repression in Savage Society.London: Rourledge & Kegan Paul Ltd.

  1. Martin, Emily. 1987. The Women in the Body: A Cultural Analysis of Reproduction. Boston: Beacon Press.
  2. Matlin, Margaret, W. 1987. The Psychological of Women. San Fransisco: Holt Rinehart and Winston Inc.
  3. McDonald, R. L. 1968. The Role of Emotion Factors in Obstetric Complications: A Review. Psychosom Med. 15 Hal 222 – 237.
  4. Moeloek, Farid, A. 1984 . Masalah-masalah Yang Mempengaruhi Kesehatan Reproduksi. Metodologi Penelitian Kesehatan Reproduksi (S. Sumapradja, dkk, ed.). Jakarta: Consortium Medical Sciences, DEPDIKBUD RI.
  5. Selby, James. et al. 1979. Psychology and Human Reproduction. London: Collier Macmillan Publishers.
  6. Sheridan, L, & Radmacher. 1990 Health Psychology, Challenging The Biomedical Model. New York: John WileY & Sons Inc.
  7. Strieder T, Wenzel B, Prummel M, Tijssen J, Wiersinga W (2003). "Increased prevalence of antibodies to enteropathogenic Yersinia enterocolitica virulence proteins in relatives of patients with autoimmune thyroid disease.". Clin Exp Immunol 132 (2): 278-82.
  8. The Bridge, Vol. 3, No. 3, Fall 1988
  9. The thyroid gland in Endocrinology: An Integrated Approach by Stephen Nussey and Saffron Whitehead (2001) Published by BIOS Scientific Publishers Ltd.
  10. Toivanen P, Toivanen A (1994). "Does Yersinia induce autoimmunity?". Int Arch Allergy Immunol 104 (2): 107-11.

Thyroid Disorders with Thyrotoxicosis


Apa yang dimaksud dengan Thyroid

Thyroid adalah sebuah kelenjar kecil, yang bentuknya seperti seekor kupu-kupu, berada di bawah leher. Yang fungsinya menghasilkan kelenjar hormon. Hormon yang dihasilkannya adalah thyroid yang terdiri triiodothyronine, T3, dan thyroxine, T4. Hormon thyroid tersebut mengatarkan energi ke sell tubuh. Warnanya merah kecoklatan, berada ditengah antara kiri dan kanan disebut juga cuping kelihatan seperti sayap kupu-kupu. Tampak jelas seperti seekor kupu-kupu dan biasanya beratnya hanya beberapa ons.

Meskipun bentuknya yang kecil, berfungsi menghasilkan thyroid, khususnya untuk yang berumur belasan tahun. Memproduksi hormon juga membantu mengontrol pertumbuhan metabolisme tubuh. Untuk menghasilkan thyroid, membutuhkan unsur kimia agar menghasilkan yoium.yang diserap dari makanan dan minuman yang kita minum. Di dalam tubuh kita terdapat 50 mg yodium. Kira-kira 1/5 sampai 1/3 di suplai (10 sampai 15 mg) thyroid disimpan di dalam tubuh. Thyroid bergabung dengan yodium untuk membuat dan menghasilkan hormon penting (asam amino esensial) dengan tyrosine.

Hormon thyroid dihasilkan dari kelenjar dan mengalir lewat sell darah dalam sell tubuh. Membantu mengontrol pertumbuhan dan struktur tulang, pertumbuhan seksual (pubertas), dan fungsi tubuh lain. Membantu sell, mengubah kalori dan oksigen untuk dapat menghasilkan energi, hormon ini amat penting untuk deteminasi tubuh. Hormon-hormon thyroid juga mempengaruhi banyak fungsi organ. Jika thyroid tidak berfungsi sebagai mana mestinya, kita akan mendapat banyak masalah dalam tubuh.

Dimana dan bagaimana kerja thyroid ?

Thyroid adalah sebuah kelenjar kecil seperti dasi kupu-kupu, tempatnya di bawah leher, terbelit pada batang tenggorok. Dibelakang atau di bawah jakun. Thyroid menghasilkan beberapa hormon, diantaranya triiodothyronine (T3) dan thyroxine (T4). Hormon ini membantu mendapatkan oksigen di dalam sell, dan membuat metabolisme kelenjar.

Hanya sell thyroid yang menghasilkan dan menyerap yodium dalam tubuh. Thyroid mengambil supplement makanan lewat yodium, melarutkan garam dalam yodium dan bergabung dengan asam amino tyrosine. Thyroid kemudian mengubah yodium dengan hormon-hormon T3 dan T4. T3 dan T4 saling berhubungan dengan molekul hormon throid.

Bila kondisinya baik, seluruh hormon diproduksi oleh kelenjar thyroid, 20% adalah T3 dan 80% adalah T4. Hormon T4 dipertimbangkan lebih kuat daripada hormon T3. Pertama kali dihasilkan oleh thyroid, T3 dan T4 dialirkan oleh darah ke seluruh tubuh. Dimaksudkan membantu sell mengubah kalori dan oksigen menjadi energi. Dikatakan thyroid, memproduksi beberapa hormon T3. Tetapi sisa hormon T3 diperlukan oleh tubuh dari banyaknya T4 yang tidak aktif sehingga dikonversi dari T4 ke T3. Konversi ini dari T4 ke T3 dapat dibuat dibeberapa organ tubuh yang lain kemudian thyroid, termasuk hypotalamus di bagian otak.

Sebagian thyroid memproses balik. Sel otak hypothalamus melepaskan Thyrotropin-releasing Hormone (TRH). Kelenjar TRH dilepaskan ke kelenjar pituitary. Thyroid Stimulating Hormone (TSH). TSH ini beredar ke aliran darah menghasilkan hormon-hormon dan mengalir ke sel darah.

Apa itu Thyroid Disease

Penyakit thyroid terjadi ketika kelenjar thyroid tidak mensuplai sejumlah hormon yang cocok.dengan tubuh. Jika thyroid over aktif, akan dihasilkan terlalu banyak hormon thyroid ke dalam sel darah, menghasilkan hyperthyroidism. (“Hyper” berasal dari bahasa Yunani, maksudnya “lebih” atau “diatas”). Hyperthyroidism dibuat di dalam tubuh dengan cepat dengan menggunakan energi, dan aktifitas kimia (seperti metabilisma) diatas kecepatan sell. Kurang aktifnya thyroid yang dihasilkan oleh hormon, menghasilkan hypothyroidism. ("Hypo" dimaksudkan "dibawah" atau "kurang.") Ketika beberapa hormon dihasilkan ke sel darah dibawah normal, tubuh menggunakan energy dengan lambat, dan aktifitas kimia (metabolisma) di dalam sell lambat. Meskipun kedua kondisi berbeda antara hyperthyroidism dan hypothyroidism thyroid menjadi lebih besar kemudian normal. Besarnya kelenjar thyroid seperti benjolan bisa di raba yang letaknya di depan leher di bawah kulit. Kalau cukup besar dapat dilihat dengan mudah, dinamakan dengan goiter. Orang yang tidak mendapatkan yodium atau kurang yodium dapat memperbesar kelenjar thyroid, tetapi langka di Amerika Serikat karena makanan disana mengandung cukup yodium.

Penyebab Thyroid Disease

Apakah yang menjadi penyebab masalah ? Ada beberapa faktor yang menjadi penyebab masalah thyroid;

  1. Kekurangan yodium dapat menyebabkan masalah thyroid.
  2. Pengobatan radiasi ke kepala, leher atau dada. Pengobatan radiasi amandel, kelenjar gondok, getah bening, kelenjar timus atau jerawat.
  3. “Terapi radium hidung”, terjadi selama tahun 1940 sampai 1960, pengobatan untuk radang amandel, pilek dan penyakit lain atau anggota militer angkatan laut, dan atau pilot yang mendapat tekanan secara drastis.

    Kelebihan mengkonsumsi makanan mentah, seperti yang di Brussel, brokoli, rutabaga, lobak turnip, kohlrabi, lobak, kembang kol, singkong Afrika, tanaman millet, babassu, kubis dan kol.

    Pengobatan pembedahan kanker thyroid, goiter atau nodules, pemindahan thyroid, meninggalkan hypothyroid.

  1. Beberapa obat, seperti lithium dan obat jantung cardarone, dapat menyebabkan hypothyroidism.
  2. Radioactive iodine treatment (RAI) untuk Graves' disease dan model hypothyroid yang ditinggalkan hyperthyroidism.
Beberapa faktor yang menyebabkan berkembangnya penyakit thyroid disease
  • Salah satu keluarga mempunyai masalah dengan thyroid
  • Salah satu keluarga terkena autoimmune disease.
  • Wanita
  • Diatas 60 tahun
  • Baru melahirkan
  • Mendekati masa menopausal atau menopause
  • Perokok
  • Terkena radiasi
  • Terkena lithium

Thyroid Disorders dan Kehamilan

Saat ini 2 % s/d 5 % penyakit thyroid disease diderita oleh wanita dan 1% s/d 2 % diantaranya wanita yang tidak produktif. Tak dapat dibayangkan, masalah thyroid banyak dialami wanita hamil. Dalam artikel ini akan digambarkan tentang kehamilan yang termasuk ke dalam masa antepartum (sebelum kehamilan) dan postpartum (sesudah kehamilan) selama kehamilan. Keduanya ibu dan anak sama pentingnya. Disini akan digambarkan dan diperkenalkan tentang thyroid disorders yang berhubungan dengan kehamilan yang banyak ditanyakan oleh pasien.

Pandangan Penyakit Thyroid pada Kehamilan

Beberapa penyakit thyroid cenderung terjadi selama masa kehamilan dengan kekebalan alami sekalipun. Ini dimaksudkan perkembangan anti bodi langsung menyerang sell thyroid, yang mana kemudian berakibat terhadap fungsi kelenjar thyroid. Anti bodi mengalami kerugian sell thyroid yang dihasilkan di lymphocytic thyroiditis (inflammation of the thyroid), juga dikenal sebagai Hashimoto's disease. Kerugian anti bodi ini akan mengurangi thyroid dan menyebabkan hypothyroidism. Tubuh kita dapat membuat anti bodi untuk melawan jaringan thyroid yang dapat menstimulasi fungsi sell thyroid. Pada kasus ini kelebihan fungsi dari thyroid hyperthyroidism (Grave disease) akan dihasilkan.

Thyroid Disease and Kesuburan

Hypothyroidism dapat juga berhubungan dengan bertambahkan masa mensturasi pasien dan rusaknya thyroid, dan tidak mengalami masa mensturasi (amenorrhea) ketika terkena hypothyroidism. Ada beberapa masalah dengan ovulasi dan kehamilan tentang hypothyroidism atau berhubungan dengan berubahnya hormon. Sebagai contoh beberapa pasien yang terkena hypothyroidism, kelenjar pituitary menghasilkan bertambahnya hormon prolactin. Bertambahnya getah prolactin dapat memberhentikan masa mensturasi. Amat jarang masalah ovarian autoimmune pada waktu yang sama dengan hypothyroidism, dengan menghancurkan anti bodi langsung menyerang jaringan. Hyperthyroidism dapat juga berhubungan dengan tidak teraturnya masa mensturasi, dan menyebabkan kurang kesuburan. Thyroid disease seharusnya dipertimbangkan pasien yang mengalami masalah mensturasi atau kurang subur. Beruntunglah keduanya diperlakukan secara memadai antara hypo- nor hyperthyroidism yang berdampak pada kesuburan.


Thyrotoxicosis berarti hormon thyroid dalam tubuh yang melebihi batas. Kondisi seperti ini juga berarti bahwa kamu memiliki TSH yang rendah dalam aliran darah, karena pituitary mendeteksi bahwa kamu memiliki hormon thyroid yang cukup. Jika kamu mengidap throtoxic, kamu merasa gugup sebab seluruh fungsi tubuhmu bergerak ke atas.

Hyperthyroidism juga diartikan sebagai kelebihan thyroid yang paling umum disebabkan thyrotoxicosis dan menimbulkan produksi kelenjat thyroid terlalu banyak. Penyebab umum hyperthyroidism adalah graves disease dimana sistem immune tidak terlalu berjalan, antibodies lemah yang menyerang thyroid sell. Proses stimulasi kelenjar thyroid menyebabkan pertumbuhan produksi hormon thyroid tinggi yang berkisar sekitar 70-80% pasien dengan hyperthyroidism mengidap graves disease dan dapat menular sekeluarga.

Sign and Symptoms

Thyrotoxicosis halus tidak dapat menyebabkan gejala apapun ketika permulaannya. Gejalanya berhubungan dengan beberapa diantaranya :

  • Kegugupan
  • Emosional
  • Mudah capek
  • Nafas pendek
  • Kurus
  • Insomnia
  • Rambut rontok
  • Kulit tipis
  • Tidak tahan terhadap panas
  • Detak jantung meningkat
  • Nyeri otot
  • Nyeri sendi
  • Sembelit
  • Kejang
  • Bengkak disekitar mata


Pencegahan untuk thyrotoxicosis akan tergantung pada umur kamu, penyebab dan beberapa dari bekas penyakit kamu, dan kondisi lain kesehatan yang pernah kamu alami. Thyrotoxicosis yang tidak dicegah dapat menyebabkan komplikasi yang serius seperti gangguan detak jantung dan oestoporosis yang dapat menyebabkan efek jangka panjang kelebihan hormon.

  • Pencegahan obat

    Dua “antithyroid” obat tersedia untuk menekan hyperthyroidism. Obat tersebut menekan production kelenjar thyroid oleh hormon thyroid. Obat digunakan untuk tujuan ini meliputi :methimazole (Tapazole) dan propylthiouracil (PTU).

    Kelompok lain dari obat yang disebut beta adrenergic blocking agents dapat mengurangi beberapa gejala thyrotoxicosis. Tingkatan hormon thyroid dalam darah bagaimanapun juga tidak menyebabkan keterlangsungan tingakan tinggi dari sirkulasi hormon pada aliran darah obat-obat ini antara lain propranolol (Inderal), atenolol (Tenormin), metoprolol (Lopressor) dan nadolol (Corgard). Mereka biasanya digunakan pada kombinasi dalam pencegahan thyrotoxicosis.

  • Yodium Radioactive

    Kamu harus memilih untuk mencegah kondisi permanen yang berbahaya pada sell thyroid dengan memproduksi hormon thyroid. Hal ini dapat menyebabkan ketergantungan dengan penggunaan yodium radioactive yang telah digunakan sejak tahun 1940. Yodium radioactive adalah perawatan yang lebih nyaman yang menggunakan kapsul cair. Sekali tercerna, ia langsung diserap dan dibawa oleh aliran darah kemudian diambil oleh sel thyroid.

  • Pembedahan

    Kamu harus merekomendasi bahwa pembedahan akan melepaskan semua bagian dari kelenjar thyroid. Kamu dapat memilih pelepasan sebagian dari kelenjar tyroid mu jika salah satu atau lebih tonjolan dari kelenjar berlebihan. Bagaimanapun juga jika tonjolan banyak masuk ke dalam kelenjar thyroid kemudian memperbanyak diri, dokter kamu harus mengeluarkan semuanya. Type pengobatan seperti ini dapat menyebabkan kondisi hyperthyroidism. Dokter kamu harus berbicara dengan kamu tentang proses dan kondisi dari pengobatan ini dan selama hal ini merupakan pilihan terbaik untukmu.