ACTH - Adrenal Gland. Discrepancy in points.

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Kaustikos

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I was listening to audio osmosis today and they happened to mention that ACTH only stimulates the release of glucocorticoids and not mineral corticoids. Kaplan and I seem to disagree on that idea and remember that ACTH stimulates all corticoids. I think this needs to be brought up.

So.

All corticoids or just glucocorticoids? Either way, someone is going to miss a question because someone didn't get their facts straight.😡
 
I was listening to audio osmosis today and they happened to mention that ACTH only stimulates the release of glucocorticoids and not mineral corticoids. Kaplan and I seem to disagree on that idea and remember that ACTH stimulates all corticoids. I think this needs to be brought up.

So.

All corticoids or just glucocorticoids? Either way, someone is going to miss a question because someone didn't get their facts straight.😡

i'm pretty sure it's all corticoids: basically glucocorticoids and mineralocorticoids. But then again, maybe someone knows more than I do about this. I could be wrong.

:luck:
 
Yeah, its both. I Just googled it and aldosterone (a mineralcorticoid) is stimulated by ACTH.
 
the above is correct, but be careful. as it was taught to me in med school, "ACTH stimulates the production and release of glucocorticoids (as well as some androgens and mineralocorticoids) from the adrenal cortex." The renin/angiotensin/aldosterone "RAA" system is the more important system for aldosterone release.
 
I really don't mean to hijack this thread, but it just reminded me of something that's been confusing me.

The hypothalamus.

Every source I use says something different or too little about the involvement of the hypothalamus with the hormones. From what I understand, it manufactures hormones in some cases, but in other cases it just gives orders to secrete the hormones. And in other cases it manufactures the hormones and gives them to a gland, and the glad is the one that secretes them. Can someone be kind enough to elaborate on this for me please?

thank you very much🙂:luck:
 
I really don't mean to hijack this thread, but it just reminded me of something that's been confusing me.

The hypothalamus.

Every source I use says something different or too little about the involvement of the hypothalamus with the hormones. From what I understand, it manufactures hormones in some cases, but in other cases it just gives orders to secrete the hormones. And in other cases it manufactures the hormones and gives them to a gland, and the glad is the one that secretes them. Can someone be kind enough to elaborate on this for me please?

thank you very much🙂:luck:

As you said, the hypo does indeed give orders as well as secrete hormones (plus a bunch of other regulation). The two direct hormones that you should be interested in are prolactin and ADH, both of which are synthesized in the hypo and then stored and released by the posterior pituitary. Additionally, the hypothalamus keeps very tight control on the anterior pituitary by the release of several tropic hormones, TRH, CRF, & GnRH. There are a few other hormones/regulators that it produces, but these are the big ones that show up on the MCAT.
 
As you said, the hypo does indeed give orders as well as secrete hormones (plus a bunch of other regulation). The two direct hormones that you should be interested in are prolactin and ADH, both of which are synthesized in the hypothalamus.
 
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You have switched oxytocin and prolactin. Oxytocin and ADH (vasopressin) are made by the neurohypophysis, transported down via neuroendocrine cells and released by the posterior pituitary via the hypophyseal portal system. Oxytocin and prolactin work with one another, but they come from different areas of the pituitary.
Bingo. Just remember that posterior stores hormones from hypothalamus and anterior makes them.

And I figured audio osmosis was wrong, I have never in my life heard that ACTH only stimulates the adrenal glucocorticoids. Thanks.
 
Bingo. Just remember that posterior stores hormones from hypothalamus and anterior makes them.

And I figured audio osmosis was wrong, I have never in my life heard that ACTH only stimulates the adrenal glucocorticoids. Thanks.

thanks for the replies

quick question: who tells anterior to make and release its hormones? the hypo? if so, how?

thanks:luck:
 
i believe that the hypothalamus makes hypophysiotrophic hormones that go through a portal system and stimulates the anterior pit to release hormones.
 
You have switched oxytocin and prolactin. Oxytocin and ADH (vasopressin) are made by the neurohypophysis, transported down via neuroendocrine cells and released by the posterior pituitary via the hypophyseal portal system. Oxytocin and prolactin work with one another, but they come from different areas of the pituitary.

You're totally right. I forgot the FLAT PEG mnemonic for the anterior pituitary. Thanks!
 
thanks for the replies

quick question: who tells anterior to make and release its hormones? the hypo? if so, how?

thanks:luck:

TRH stimulates the ant pit to release TSH
CRF stimulates the ant pit to release ACTH
GnRH stimulates the ant pit to release LH & FSH
 
Oxytocin and ADH (vasopressin) are made by the neurohypophysis, transported down via neuroendocrine cells and released by the posterior pituitary via the hypophyseal portal system. Oxytocin and prolactin work with one another, but they come from different areas of the pituitary.

Oxytocin and vasopressin are primarily produced within the paraventricular and supraoptic regions of the hypothalamus, not the neurohypophysis. They do not come from different areas; they are found in both regions although there is more oxytocin in the paraventricular, and more vasopressin in the supraoptic. The same neurons that produce the hormones extend processes down into the neurohypophysis. This is the hypothalamo-hypophyseal tract, not the hypophyseal portal system (which refers to the vascular flow from hypothalamus to adenohypophysis). Oxytocin and prolactin do not work with each other, although they are associated with childbirth and lactation. Oxytocin controls smooth muscle contraction and milk let down. Prolactin controls breast development and milk production. No overlapping functions.
 
Oxytocin and vasopressin are primarily produced within the paraventricular and supraoptic regions of the hypothalamus, not the neurohypophysis. They do not come from different areas; they are found in both regions although there is more oxytocin in the paraventricular, and more vasopressin in the supraoptic. The same neurons that produce the hormones extend processes down into the neurohypophysis. This is the hypothalamo-hypophyseal tract, not the hypophyseal portal system (which refers to the vascular flow from hypothalamus to adenohypophysis). Oxytocin and prolactin do not work with each other, although they are associated with childbirth and lactation. Oxytocin controls smooth muscle contraction and milk let down. Prolactin controls breast development and milk production. No overlapping functions.

And that, children, is WAY beyond the scope of the MCAT. Minus the last bit about prolactin and oxytocin. And doesn't oxytocin play a part in orgasms?😛
And thanks for that clarification.

And the best way to remember what controls anterior release, honestly, is to just know that they have "releasing" in them. They themselves are contrlled by hormones. If anything, it helps to just know that the posterior is a storage depot and isn't stimulated by any release hormones and that the anterior is.

CRH
GHRH
GnRH
TRH
See the pattern? The more important thing to know, imo, is how they interact overall, even including the negative feedback mechanism.

ie; why do you get goiter formation in both hyper and hypothyroidism?
 
Wild guess:

Hyperthryoidism will see goiter formation because of increased levels of thyroid hormone output. Hypothyroidism will see goiter formation because of decreased levels of negative feedback on the hypothalamus and anterior pituitary leading to high levels of TSH which "tries" to stimulate the thyroid to produce--maybe I deficiency would have to be the cause in this case?

😀
 
Wild guess:

Hyperthryoidism will see goiter formation because of increased levels of thyroid hormone output. Hypothyroidism will see goiter formation because of decreased levels of negative feedback on the hypothalamus and anterior pituitary leading to high levels of TSH which "tries" to stimulate the thyroid to produce--maybe I deficiency would have to be the cause in this case?

😀
Not bad...But why isn't there the negative feedback in hyperthyroidism? I would assume that it wouldn't form a goiter because of the negative feedback. But, then again, if the negative feedback were working, there wouldn't be increased serum [I-]...I guess it does make sense. Thanks tncekm!
 
Maybe there is something wrong with the thyroid hormone receptors in the hypothalamus / anterior pituitary?

I dunno, like I said, it was just a wild guess 😀
 
Maybe there is something wrong with the thyroid hormone receptors in the hypothalamus / anterior pituitary?

I dunno, like I said, it was just a wild guess 😀

Hypothyroidism leads to goiter because of insufficient triiodothyronine and thyroxine, which causes loss of negative feedback on TSH secretion. This is the classical case of goiter development.

Hyperthyroidism when caused by Graves' Disease will also cause goiter. I believe this is due to autoimmune response to TSH receptors in the thyroid gland, where the antibody created ends up attaching to the binding site of the receptor. This causes excessive thyroid activity and goiter.
 
hypo
1) Failure of thyroid gland or lack of iodine ---> TSH increases (tropic hormone from AP that normally stimulates thyroid gland to release T3 T4, but since thyroid gland is failing no thyroid hormone(T3 T4) so no neg feedback on anterior pituitary) so TSH still increase ----> goiter

hyper
1) eg Graves Disease (lots of long acting thyroid stimulators so T3 and T4 increase, however LATS not subject to neg feedback by the thyroid hormones so thyroid keeps growing ---> goiter

there are more situations but i hope this helps or makes sense....
 
Hypothyroidism leads to goiter because of insufficient triiodothyronine and thyroxine, which causes loss of negative feedback on TSH secretion. This is the classical case of goiter development.

Hyperthyroidism when caused by Graves' Disease will also cause goiter. I believe this is due to autoimmune response to TSH receptors in the thyroid gland, where the antibody created ends up attaching to the binding site of the receptor. This causes excessive thyroid activity and goiter.


Yeah, but I was never quite sure why TSH receptor attack caused the goiter. They told me the mechanism was unknown. I just remembered hyper as that or cancer formation.:idea: The follicular cells become cancerous and increase in number, thus goiter. But that may be taking the easy way out.😀
 
Hypothyroidism leads to goiter because of insufficient triiodothyronine and thyroxine, which causes loss of negative feedback on TSH secretion. This is the classical case of goiter development.

Hyperthyroidism when caused by Graves' Disease will also cause goiter. I believe this is due to autoimmune response to TSH receptors in the thyroid gland, where the antibody created ends up attaching to the binding site of the receptor. This causes excessive thyroid activity and goiter.

Ahhh, cool. I guess I was somewhat heading in the right direction 😳
 
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