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Can someone explain how goiters occur in both hypo and hyperthyroidism?

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auburnO5

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So iodine deficiency results in increased iodide trapping -> goiter, right?

Which leads to hypothyroidism -> cretinism ?


How exactly does hyperthyroidism relate to a goiter?

Thanks!
 

mdeast

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Goiter just means enlarged thyroid. The thyroid can be physically enlarged either in cases of overproducing or underproducing T3/T4.
 

amaprez

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Like mdeast said, having a goiter itself is not diagnostic of anything. You need to determine if it's Hypo or Hyperthyroid. And cretinism only applies if we're talking about babies.
 

COdoubleMO2theN

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Hypo: increased TSH leads to gland hypertrophy.

Hyper: overproduction of colloid leads to enlargement.

I believe this is right - its how I reasoned it anyway.
 

mdeast

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Hypo: increased TSH leads to gland hypertrophy.

Hyper: overproduction of colloid leads to enlargement.

I believe this is right - its how I reasoned it anyway.

There are a lot more causes than that (i.e. neoplasm, infectious, autoimmune, etc. that will increase the size via different mechanisms and in different ways...i.e. the whole thing, nodular pattern, etc.). They hypo/hyper state can just be a result of some other process happening. Read First Aid :)
 

COdoubleMO2theN

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There are a lot more causes than that (i.e. neoplasm, infectious, autoimmune, etc. that will increase the size via different mechanisms and in different ways...i.e. the whole thing, nodular pattern, etc.). They hypo/hyper state can just be a result of some other process happening. Read First Aid :)


Obviously there is but they were referring to iodine deficiency for hypo and I assumed graves (most common) for hyper which is how I answered the question. Be easy with that read first aid comment bud - I answered the why not the what as you just did.
 

Pills Of Soap

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Hypo: increased TSH leads to gland hypertrophy.

Hyper: overproduction of colloid leads to enlargement.

I believe this is right - its how I reasoned it anyway.

For the OP, to further expand, in Graves, the auto antibody is stimulating the TSH receptor (like the same way the increased TSH stims the receptor in hypothyroidism)
 

mdeast

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Obviously there is but they were referring to iodine deficiency for hypo and I assumed graves (most common) for hyper which is how I answered the question. Be easy with that read first aid comment bud - I answered the why not the what as you just did.

The read First Aid wasn't targeted at you. It was targeted at the OP. He should read First Aid to find out these answers.

And no, I don't think the OP was asking about Graves and iodine deficiency. I think he didn't realize what goiter really was.
 

auburnO5

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I know what a goiter is. And I've read FA four times.

It's just a little puzzling to me that a goiter can be associated with both hypo and hyperthyroidism, so I was looking for a somewhat simple answer.
 

DrDJShik

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Basically, as stated earlier the Stimulation of the thyroid gland is responsible for its increase in size. So if you aren't making enough T4 as in iodine deficiency (hypo-), the negative feedback of T4 on the pituitary stops and more TSH is released causing the thyroid to grow in size (Low T4, high TSH). Same with hyper- when TSH-like receptor agonists (Ab) as in Graves disease stimulate the thyroid to work harder increasing its size (high T4, low TSH)
 
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MudER

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.Goiter is just an enlargement of thyroid gland due to impaired synthesis of thyroid hormones. ..Thyroid hr deficiency .-->.↑↑ ..TSH --> ..hypertrophy and hyperplasia of thyroid follicular cells .--> .thyroid enlargement..
.In my understanding, not all goiters cause hypo/hyperthyroidism, as a matter of fact most pts with goiter r euthyroid. . .Below is how I reason with goiter and how hypo/hyper r related to goiter. .

.Iodine deficiency is associated with the diffuse nontoxic/simple goiter (the endemic type). Remember there r two types of goiter (diffuse nontoxic/simple goiter, and multinodular goiter). MNG arises from simple goiters due to recurrent episodes of hyperplasia and involution .-->.Irregular enlargement and nodularity of the gland. Majority of diffuse nontoxic goiter pts r euthyroid: T3 and T4 normal, TSH (mildly elevated), and the symptoms r due to mass effect. .
.In MNG, there r two types: nontoxic (majority), and toxic MNG. The toxic MNG --> ..thyrotoxicosis (Plummer’s disease). Therefore, ..most patients with multinodular goiters are also euthyroid, but the toxic type may contain a solitary or multiple hyperfunctioning hot nodules .--> .thyrotoxicosis (which is one of the causes of hyperthyroidism)..

.All these r in Goljan. .
 

sylvanthus

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lol amuses me that OP was looking for a simple response and people bust out all the stops about all the negative feedback loops etc.

OP just think of it like this. In hyperthyroidism the tissue is hyperfunctioning and enlarges because of it. In hypothyroidism, the tissue that is still normal has to hyperfunction and enlarge to make up for the underproducing tissue. Whether this is entirely correct or too simplified doesn't really matter, it helps it stick.
 

auburnO5

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lol amuses me that OP was looking for a simple response and people bust out all the stops about all the negative feedback loops etc.

OP just think of it like this. In hyperthyroidism the tissue is hyperfunctioning and enlarges because of it. In hypothyroidism, the tissue that is still normal has to hyperfunction and enlarge to make up for the underproducing tissue. Whether this is entirely correct or too simplified doesn't really matter, it helps it stick.

Thanks. This is what I was looking for.

I can't believe the guy that busted out "Read First Aid." :laugh:
 

mdeast

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Thanks. This is what I was looking for.

I can't believe the guy that busted out "Read First Aid." :laugh:

LOL. It's not as simple as that though. You could have infectious, neoplastic, fibrotic, etc. processes that involve the thyroid that have nothing to do with Graves or Iodine deficiency that will still cause signs of hypothyroidism or hyperthyroidism with goiter. You need to know all of these for Step 1. In other words, TSH stimulation may not be the real reason that the thyroid is enlarged in a hypo-thyroid state. By simplifying it too much, you're not learning what you need to know for Step 1.
 

Charles_Carmichael

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lol amuses me that OP was looking for a simple response and people bust out all the stops about all the negative feedback loops etc.

OP just think of it like this. In hyperthyroidism the tissue is hyperfunctioning and enlarges because of it. In hypothyroidism, the tissue that is still normal has to hyperfunction and enlarge to make up for the underproducing tissue. Whether this is entirely correct or too simplified doesn't really matter, it helps it stick.
The way I learned it (and an easier way to remember it, IMHO) is that stimulation of the TSH receptor on the thyroid gland has a trophic effect.

In the case of hypothyroidism, you don't have negative feedback from T3/T4 on the anterior pituitary, so the anterior pituitary is producing more TSH. TSH keeps stimulating the TSH receptor leading to hypertrophy/hyperplasia of the follicular cells --> you have a goiter!

In the case of hyperthyroidism, for example from Graves disease, you have autoantibodies stimulating the TSH receptor. This stimulation of the TSH receptor activates the pathways leading to hypertrophy/hyperplasia and the formation of a goiter.

Hope this helps.
 

auburnO5

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LOL. It's not as simple as that though. You could have infectious, neoplastic, fibrotic, etc. processes that involve the thyroid that have nothing to do with Graves or Iodine deficiency that will still cause signs of hypothyroidism or hyperthyroidism with goiter. You need to know all of these for Step 1. In other words, TSH stimulation may not be the real reason that the thyroid is enlarged in a hypo-thyroid state. By simplifying it too much, you're not learning what you need to know for Step 1.

I should have never asked this question. :bang:
 
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