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Thyroid Disease

The thyroid is under control from the pituitary gland which puts out TSH that stimulates the thyroid to secrete predominantly T4 thyroid disease, hypothyroidism, hyperthyroidism. T4 then can be converted to T3 as needed and so what is active mostly at the tissue level is T3 but very little of T3 is actually made by the thyroid. Most of that is made in the peripheral circulation because of the effects of deiodinase. Deiodinase activity is completely regulated independent of thyroid function so that measuring T3 in most cases does not help.

Hypothyroidism. By far, this is the most common. Weíre talking about 2% of all hospitalized patients. Estimates of 5-7% in the general population above the age of 55, 10% of those diagnosed with depression and 0.5% of all psychiatric admissions. So, itís a common disorder. There have been some recommendations even for doing general screening because it so common but certainly anyone with depression should be screened for hypothyroidism.

Euthyroid Sick Syndrome. Essentially everyone who is in the hospital who is ill probably has some features of euthyroid sick. This is a person who is clinically euthyroid and yet it sometimes is very difficult to identify that when someone is intubated, comatose and edematous.

What we do know also is that if we overtreat, and we did a lot of overtreatment before we had this good TSH assay to be able to distinguish hyperthyroidism from euthyroidism, we cause osteopenia. We actually decrease bone density. We knew a long time ago that people on thyroid were at increased risk for osteoporosis but we didnít know why. Now we know why and if the TSH is in the normal range, we donít cause osteoporosis and if someone has decreased bone density and their TSH is too low and they get it into normal range, then they will, in fact, have recruitment of osteoblasts and they will regain some of that bone density.

Hyperthyroidism is not as common as hypothyroidism but it isnít totally uncommon. In fact, we think of it as a young personís disease but 20-30% of it occurs after the age of 60. So elderly are not immune from developing hyperthyroidism. The key in the elderly, I want to talk to this point, because you probably have all seen young people with hyperthyroidism but the older person is less likely to have the classic presentation. 75% will but 25% will be an abnormal presentation such as anorexia, weight loss, muscle strength problems or failure to thrive. So they just donít feel good, they donít look good and they can present with cognitive impairment, decreased concentration, confusion or agitation.

Thyroiditis, you have to appreciate that there are several different kinds. Acute bacterial, we almost never see in this country so you donít have to worry about that. Radiation induced. You almost always know that they just had it so that shouldnít be a problem either. So really weíre left with these three: Subacute lymphocytic and in the literature you can sometimes see it called painless or silent. It was called a lot of different things before they agreed that this should be the preferred term. Subacute granulomatous which used to be called just subacute before we found out there are a couple of different kinds or de Quervainís. You might have heard of that also. Then chronic lymphocytic which is the same thing as Hashimotoís. Now, Hashimotoís we know causes hypothyroidism but if thereís a lot of active inflammation in Hashimotoís, you can have a burst of hyperthyroidism before they actually become hypothyroid. So Hashimotoís can do both but itís mostly these other ones that are probably as, or more common, than Hashimotoís thyroiditis.

The painless or silent thyroiditis is autoimmune like everything else. We think that it may be set off by a virus but it may also be set off by a stress. The situation where we see it most commonly is postpartum. Itís the same thing as postpartum thyroiditis.

Subacute thyroiditis, de Quervainís. Sometimes this is called subacute granulomatous thyroiditis because if you stick a needle in you get a granuloma. Again, female predominance. We do believe, for sure, that although there is an autoimmune component this is a virally mediated disease. It causes inflammation in the gland. Oftentimes youíre going to have an antecedent history of an upper respiratory infection. They sometimes will have a fever or had a fever and the key is the gland is tender in this particular case. The thyroid generally is not overly large. There is some thyromegaly but not overly large.

Generally, if I think itís tender and the setting is right, I donít even do the sed rate and white count to confirm that because you have the appropriate setting, assuming that the thyroid function tests match.

Hashimotoís thyroiditis. At a period of time where they have more active inflammation you can have a period of high thyroid function. Their antibodies could be elevated but they donít have to be. The gland in this particular case, whether itís in chronic hypothyroidism or in this hyperthyroid phase, is more likely to be irregular, firm, a lot of scarring going on in that gland.

They can sometimes have the Gravesí ophthalmopathy too. So there is some overlap there and they might have multiple periods of time of these hyperthyroid phases as you can have also with the painless and the subacute granulomatous or the tender thyroiditis.

The course is variable. In general, you observe them and we can talk a little bit more about other treatments.

So how do you treat hyperthyroidism? It depends on the cause. Again, you can use symptomatic treatment in anyone. Beta blockers help with the tremor and the tachycardia and make people feel better but Gravesí disease and multinodular goiter.

Gravesí disease, you have really three options as you do for all of them but we tend to use just two. The thioamides or radioactive iodine. You can do surgery and weíll talk about that in a minute but the cost and the morbidity is potentially much higher. Thioamides are only going to be effective 50% of the time basically in the end and the people in who these are most likely to be effective by themselves are people who have had recent onset and small goiters. Not very symptomatic. If they have a big gland, itís been sitting there for a long time, you might as well forget it because they are not going to be cured with thioamides alone.

The advantages of trying thioamides is you are less likely to have hypothyroidism, initially, after treatment. They certainly can be The disadvantages are it is more likely to result in hypothyroidism. There is no absolute dose that you can be sure that youíre going to get rid of the hyperthyroidism and not develop hypothyroidism and a lot of people get real anxious when they hear the term "radioactivity". Like in Japan, they almost never use radioactive iodine. You can imagine why and, ultimately, they do a lot of surgery in Japan for thyroid disease.

There is some question about whether radioactive iodine exacerbates Gravesí ophthalmopathy. There is one paper that says it does and other papers that say it doesnít. In the end I donít think that that is definitively concluded but I donít think thereís enough evidence to say that we shouldnít use it in people who have Gravesí ophthalmopathy.

If they are on the antithyroid drugs. However, before they go to radioactive iodine, I frequently will start someone on antithyroid drugs even if I am going to go to radioactive iodine in order to get their thyroid hormone ratio down so that they are less symptomatic right away and less likely to have an exacerbation at the time of getting the radioactive iodine. So it doesnít mean that you canít use the two together but the key is that they have to go off the drug before they get the radioactive treatment. PTU has a shorter half-life and so you have to go off at least 48 hours for that one. Methimazole has a longer half-life Ė at least five days for that one. The key is PTU.

Now, there is an advantage of anyone who is pregnant being on PTU over methimazole because there is some question about binding that there is greater protein binding, so itís less likely to cross the placenta.

Surgery can be used in Gravesí disease especially if you have a nodule that you think is suspicious, they failed thioamides because of compliance issues or they are pregnant and have failed. The disadvantages are cost or morbidity.

Multinodular goiter. It requires treatment. In this particular case, you can use the thioamides, again, to get them prepared but it will never cause them to go into remission. It is not a long term treatment for multinodular goiter. We already talked about 

Thyroiditis. Again, a self-limited course. No treatment required other than beta blockers. In the case of subacute thyroiditis and granulomatous thyroiditis, you can use anti-inflammatory agents.

So, just a little review, and this in your handout. Causes of hyperthyroidism. Again, they are pretty much younger age group with the exception of toxic nodules and multinodular goiter. It doesnít mean that these canít occur in older age groups but in general, they tend to be younger. They are all female predominant. The thyroid helps you diagnose the individual causes. Gravesí disease, you expect a symmetric, larger type goiter. Subacute thyroiditis that is the tender type is a small tender goiter. Silent thyroiditis, a small nontender goiter and toxic nodule, multinodular goiter is an asymmetric gland generally with one or more firm nodules.

Thyroid cancers. By far and away the most common is papillary thyroid carcinoma. It turns out itís also the most benign and in general, these individuals, if treated properly, really have no difference in life span of people who donít have papillary thyroid carcinoma.

Follicular carcinoma is the second most common and the second most benign and itís also differentiated so it does respond to treatments that we use for papillary as well.

Medullary thyroid carcinoma is the fourth in frequency but the third in terms of its malignancy. However, it is very slow growing so even though a lot of these individuals present with metastatic disease, they sometimes can live 5, 10, 20 years after 

The undifferentiated thyroid carcinomas, anaplastic, etc. as the third most common and the worst in terms of outcome. There is almost nothing you can do that is going to change their outcome of dying probably within 12-14 months. So regardless 

Papillary thyroid carcinoma. The key is whether you are talking about papillary thyroid carcinoma or follicular you want to get out the tumor, ablate the remainder and then put them on thyroid hormone. Thatís sort of the theme of thyroid cancer. You want 

Follicular thyroid carcinoma. Even more important than papillary, you need to get out all the thyroid gland and ablate the remnant in order to identify if they have metastatic lesions. Youíre more likely to have hematogenously spread metastases with follicular carcinoma. So you have to get out the thyroid, ablate the remnant and then come back when they are hypothyroid to

Thyroglobulin is a blood test you can use for either papillary or follicular as a tumor marker that you can measure on regular intervals to determine the response of the disease mass, if you will. Weíve found out since, that it turns out you donít have to do it when they are hypothyroid. If it starts going up, you know that the tumor is growing. Again, thyroid replacement will be

Anaplastic thyroid cancer. Again, life expectancy very dim. External beam radiation is about as much as you can do and some kinds of palliative surgery.

Medullary thyroid cancer. The key is that you have to recognize that this could be part of an inherited syndrome and you may want to screen other family members for aspects of the syndrome. Sometimes you can pick them up early before they actually develop the tumor and

So, thyroid cancer is TSH responsive. You want to minimize TSH to stimulate thyroid growth and monitor their replacement very carefully with TSH