Graves Disease - confusion regarding feedback inhibition

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

foxi

Full Member
7+ Year Member
Joined
Dec 17, 2015
Messages
35
Reaction score
0
taking a practice exam and got this problem wrong:

"Graves’ disease is an autoimmune disorder in which autoantibodies are formed against thyroid stimulating hormone (TSH) receptors on the thyroid gland. Patients with Graves’ disease present with resting heart rates of 105-120, elevated body temperature, increased appetite, weight loss, and insomnia. Which of the following hormone levels would be expected in a patient with Graves’ disease?"

a) decreased TSH, decreased Thyroxine (T3/4)
b) decreased TSH, increased Thyroxine (T3/4)

Answer is B.

Problem is I can reason this two ways, both of which make sense to me:
1) Autoantibodies remove TSH, which stimulates T3/4 production. Thus, removing TSH will reduce total amount of T3/4.
or
2) Looking at the patients symptoms, we see that he/she has a higher metabolic rate, which results from increased levels of T3/4, which would then negatively feedback onto the pituitary to prevent more TSH from being produced.

What is wrong about my reasoning?

Thanks!

Members don't see this ad.
 
I am confused as to what your question is. You gave 2 reasonings, are you asking which one is wrong?

If so,

1 is incorrect because the antibodies do not destroy TSH. they destroy TSH receptors on the thyroid gland.

So you will have more free floating TSH in the body and this will negatively feedback on the pituitary.
 
I am confused as to what your question is. You gave 2 reasonings, are you asking which one is wrong?

If so,

1 is incorrect because the antibodies do not destroy TSH. they destroy TSH receptors on the thyroid gland.

So you will have more free floating TSH in the body and this will negatively feedback on the pituitary.

->>>Sorry I didn't specify.. I was wondering why 1 is incorrect. Even so: whether it be destroyed TSH or destroyed TSH receptors, the effect would be the same, in that there will be less Thyroxine.
 
->>>Sorry I didn't specify.. I was wondering why 1 is incorrect. Even so: whether it be destroyed TSH or destroyed TSH receptors, the effect would be the same, in that there will be less Thyroxine.

I thought so to, but the symptoms line up with excess T3, T4 so that would be the better choice I suppose.

I really don't know why the answer beyond that :(

Edit. FOund the answer!

In Graves’ disease, your immune system creates antibodies that cause the thyroid to grow and make more thyroid hormone than your body needs. These antibodies are called thyroid-stimulating immunoglobulins (TSIs). The TSIs bind to thyroid cell receptors, which are normally “docking stations” for thyroid-stimulating hormone (TSH—the hormone responsible for telling the thyroid to produce hormones). The TSIs then trick the thyroid into growing and producing too much thyroid hormone, leading to hyperthyroidism.
 
Members don't see this ad :)
I thought so to, but the symptoms line up with excess T3, T4 so that would be the better choice I suppose.

I really don't know why the answer beyond that :(

Edit. FOund the answer!

In Graves’ disease, your immune system creates antibodies that cause the thyroid to grow and make more thyroid hormone than your body needs. These antibodies are called thyroid-stimulating immunoglobulins (TSIs). The TSIs bind to thyroid cell receptors, which are normally “docking stations” for thyroid-stimulating hormone (TSH—the hormone responsible for telling the thyroid to produce hormones). The TSIs then trick the thyroid into growing and producing too much thyroid hormone, leading to hyperthyroidism.
->>> ah.. don't know how I was to know that but thanks! I guess I should have looked at the patients symptoms more closely. I thought that they were there to distract me..
 
[oops. my answer comes a little too late I guess :)]

The autoantibodies do not 'destroy' anything! They're just capable of binding the TSH-receptor and thus activating it! So they basically do the very same thing as TSH itself: activating the thyroid gland, leading to increased levels of T3 and T4. The TSH-levels decrease, because T3/T4 inhibit the TSH secretion in the pituitary gland (negative feedback mechanism).
 
  • Like
Reactions: 1 user
about the antibodies, i dont understand why there's no destruction of the tsh-receptor if we have formation of inmune-complex (TSH-receptor---TSI) in the graves disease.
whats the difference between the antibodies on graves and hashimotos disease that leads in the first case to the stimulation of the glandule and in the second one to the destruction of it?
 
about the antibodies, i dont understand why there's no destruction of the tsh-receptor if we have formation of inmune-complex (TSH-receptor---TSI) in the graves disease.
whats the difference between the antibodies on graves and hashimotos disease that leads in the first case to the stimulation of the glandule and in the second one to the destruction of it?

From my understanding, Grave's disease is a disease where the body produces antibodies - specifically, thyroid-stimulating antibodies. As mentioned, these antibodies will act in the same way that TSH does. They bind to the TSH receptor, stimulate the thyroid to produce T3/T4. The increase in T3/T4 causes negative feedback back to the hypothalamus and the pituitary; causing a decrease in the amount of TRH and TSH. However, the antibodies will still keep stimulating that TSH receptor and the thyroid will still keep producing T3/T4. It makes sense why, in patients with Graves Disease, you will see LOW levels of TRH/TSH (due to negative feedback) and high levels of T3/T4 (due to the antibodies stimulating the TSH receptors). You will see symptoms of HYPERthyroidism (high heart rate, increased metabolism, etc etc)

In Hashimoto's disease, the immune system sees the thyroid gland as a foreigner and starts attacking it. It is more characteristic of the typical auto-immune diseases out there - the immune system will destroy the thyroid, leading to low levels of T3/T4. These low levels will tell the hypothalamus and pituitary to secrete more TRH/TSH, but no matter how much they secrete, the thyroid won't be able to make T3/T4. I believe in this case you would see HIGH levels of TRH/TSH and low levels of T3/T4. The symptoms associated with Hashimoto's will be that of HYPOthyroidsim (low heart rate, low metabolic rate leading to weight gain, etc).

They seem to only differ in the specific response the immune system has against the thyroid (stimulating the thyroid in one and attacking it in the other). Hope that makes sense :)
 
Top