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Old 04-14-2012
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Default Hyperthyroidism & Hypothyroidism

In Graves disease (hyperthyroidism), the characteristic findings are exophthalamos and peritibial myxedema. That is because behind the eye and in the tibia there are TSH receptors ... (not sure about this) and once the autoantibodies bind to the TSH receptors they produce GAG's (glycosaminoglycans) which lead to the findings of exophthalamos and pertibial myexedema.

In hypothyroidism, there are increased levels of TSH because of lack of negative feedback. Shouldn't you see the same signs as Graves disease (the exophthalamos and peritibial myxedema) in hypothyroidism as well ?

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Old 04-14-2012
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Where did you read about TSH receptors being behind the eyes? It doesn't pass the sniff test. No doubt, there is an increase in GAGs, but I don't think the mechanism is because of TSH receptors.

I could be wrong, though.
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i think he got that mechanism from pathoma
because thats my understanding of it too

but then i got confused when they said u have myxedema in hypo as well
but it makes sense, because in hypo u have increased TSH
dont know why hypo doesnt affect the eye, but it does cause myxedema.
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The etiology of the thyroid-related orbitopathy is an autoimmune-mediated inflammatory process of the orbital tissues, predominantly affecting the fat and the extraocular muscles. Lymphocytes, plasma, and mast cells are the cellular constituents in this process. The deposition of glycosaminoglycans and the influx of water increase the orbital contents. Obstruction of the superior ophthalmic vein with resultant diminished venous outflow also contributes to the orbital engorgement.
Nunery has segregated patients with thyroid-related orbitopathy into type I and type II.[2] Those with type I do not have restrictive myopathy, whereas those with type II do. Type I was believed to be caused by a profundity of hyaluronic acid manufactured by the orbital fibroblasts, stimulating lipoid hyperplasia and edema. Patients with type II experience restrictive myopathy and have diplopia within 20° of fixation.
Orbital emphysema can be a significant cause of proptosis and requires emergency treatment.


SOURCE: eMedicine
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Quote:
Originally Posted by Valkoff View Post
Where did you read about TSH receptors being behind the eyes? It doesn't pass the sniff test. No doubt, there is an increase in GAGs, but I don't think the mechanism is because of TSH receptors.

I could be wrong, though.
I heard it in the Pathoma videos!

His exact words -

"They (patients of Gave's dx) get exophthalamos and pretibial myexdema. This is high yield and you should know that this is not due to hyperthyroidism. It is due to the fact that patients have an Antibody that stimulates the TSH receptors. So the idea here is that the fibroblast's behind the eye and the fibroblasts over the shin have TSH receptors and so in response to the AB's they begin to secrete excess GAG's"


Quote:
Originally Posted by Valkoff View Post
The etiology of the thyroid-related orbitopathy is an autoimmune-mediated inflammatory process of the orbital tissues, predominantly affecting the fat and the extraocular muscles. Lymphocytes, plasma, and mast cells are the cellular constituents in this process. The deposition of glycosaminoglycans and the influx of water increase the orbital contents. Obstruction of the superior ophthalmic vein with resultant diminished venous outflow also contributes to the orbital engorgement.
Nunery has segregated patients with thyroid-related orbitopathy into type I and type II.[2] Those with type I do not have restrictive myopathy, whereas those with type II do. Type I was believed to be caused by a profundity of hyaluronic acid manufactured by the orbital fibroblasts, stimulating lipoid hyperplasia and edema. Patients with type II experience restrictive myopathy and have diplopia within 20° of fixation.
Orbital emphysema can be a significant cause of proptosis and requires emergency treatment.


SOURCE: eMedicine
Thanks. Still confused about why we don't see that in patients with hypothyroidism.
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I'm guessing that the antibodies in Graves cross react with orbital tissues; while the ones in Hashimoto's are not molecularly similar.

It is a very good question, though. I'm stumped.
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