endooo

[xinester]

Has anyone out there taken endocrinology? Final tomorrow ugh and I'm wondering why long-term glucocorticoids cause osteoperosis. Also, why are GCC's a good treatment for asthma? Because it's anti-inflammatory ?.....

sinistera. You are not on AIM, so I write this, hoping you will answer. I know you must knowwww everythinggg waghhh haaalpp meee ;^;

Comments

[joobley]

Long-term GCC causes osteoporosis via Cushing's syndrome, which includes acceleration of bone loss. '_'

and yes, GCC's are effective for asthma because it is anti-inflammatory. Asthma is an autoimmune disorder acquired in childhood (before age 7 I think??) that results in remodelling of the respiratory tract, which results in hypersensitivity to certain stimuli.

I wonder if this helps : D;

[xinester]

But bone loss how????? DDDDDDDDD:

And I guess my second question was a little more specific--I was just wondering why GCC's work for asthma attacks since epinephrine is also a treatment for asthma but works in a different way (it's inhibiting MLCK and dilates the bronchi). But then, all GCC's due is act as an anti-inflammatory. I guess I don't really know what asthma attacks really entail, I guess some kind of inflammation and muscle blockage?

[joobley]

GDI LOL
I just know it's impaired osteoblasts but normal osteoclasts... ;v;lll

As for GCC's fxn, it's used for maintenance (I guess prevention), not as Tx for acute attacks like epi is.

[sinistera]

This is what I remember and ... what my book tells me

1. Asthmatics have a low number of beta-adrenoceptors in their bronchial smooth muscle.
2. As you've mentioned, stimulated beta-ARs relaxes bronchial smooth muscle. This is to increase air flow during flight-or-fight.
3. You can ... probably piece together the rest.

Basically, GCCs act on the immune system while catecholamines act on the muscle. Remember that GCCs always induce relatively longer term responses while catecholamines are for immediate, and usually short responses.

[sinistera]

O-okay I'll attempt this but hang on a sec so I can gather my thoughts. ;w;

[sinistera]

Okay, I can answer the second one more readily because I know off the top of my head that initially, the HPA axis activates the immune system, and then inhibits it. From what I can understand, IL-1 (a cytokine) stimulates ACTH release, which then stimulates GC production and release, which then inhibits the lymphatic system. Therefore, it's like a negative feedback to bring the immune system back to stability.

It's not exactly clear how GC suppresses the lymphatic system. It might be that GCs stop leukocytes from reaching the infected tissue or or ... something. I don't know. However, chronic stress has been known to cause atrophy of lymphatic organs.

[xinester]

Yeah, sooo cytokines act back at the hypothalamus and increase CRH&AVP -> increase ACTH -> negative feedback onto the APC to decrease immune system/degranulation of mast cells -> anti inflamm... and that's it? I was wondering what that had to do with Asthma though like, how could both epi and GCC's be a treatment for asthma when they're doing two different things? I was wondering if GCC's were possibly doing something else, but if not, that's cool :P Will just have to live with it.
You are so knowledgable bb, thank you for helping! Sorry I missed your AIM messages, I was at my friend's house studying and I forgot to turn off the computer ;3;

[sinistera]

Ummm... I'm not really familiar with how elevated GCs trigger osteoporosis but this is what my book tells me:

1. GCs break down skeletal muscle.
2. Loss of the protein matrix around the muscle leads to osteoporosis.
3. Over time, the spinal column is affected.

I have no idea how GCs breaks down skeletal muscle. I want to say that it involves insulin (in Cushings, elevated GCCs in the blood is translated to hyperglycemia by the body, when then wears our pancreatic beta-cells so they can't respond to insulin), but I don't know how insulin affects protein catabolism.

[xinester]

BBBBBBBBBBBBBB you are wonderfullll ;3; thank you for trying to answer! I ended up calling one of my friends who told me the answer was in the last few lectures of our class (which I skipped lol) and you are right. GCCs break down skeletal muscle via increasing osteoclast activity (ODF receptor maybe? Ionno) and decreasing osteocyte activity. Matrix gets broken down and voila! Thank youuuu bbbbbbbbbbbbb ;____________________;

[xinester]

Oh, random but, do you have any idea why intermittent PTH causes bone formation and continuous PTH causes resorption then osteoperosis?

I have a diagram of bone and osteoblast+osteoclast; osteoclast has an ODF receptor, lysosomes w/ cathedsin K, protons (all to break down bone); osteoblast has a PTH receptor, when activated it synthesizes ODF.

So PTH -> PTH R -> ODF -> ODF R -> release cathed K & protons -> degrade local bone

I feel like it should be plain and simple, ODF causes osteoperosis? Why would it ever promote bone growth?? D:

[joobley]

oh and soon

"endooo"

will have a whole new meaning to you since you're in dentistry :D

[xinester]

endodontics, you mean ? hehe, I work in an endodontics research lab akshully 8D i just thought no one would notice if i used endo for endocrinology lololol ;) clever one !

[joobley]

Oh wow! Chups you are so cool!! I love scientists X)