mdwannabe
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Cortisol directly stimulates osteoclasts, so serum Ca goes up, but most of that Ca will be bound and excreted, so in actuality the patients with Cush do not suffer from Hyper Ca.
Cortisol does have weak mineralocortic activity, so K levels may drop down, but since high Corisol reduces ACTH the adrenals degenerate and may cause hypo Aldo, which will probably counterballance the K levels.
In any case, nither level is diagnostic or helfull in disease. Always correlat with rest of clinical presentation.
Thats my opinion.
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| Bunny
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"mdwannabe" wrote:
... but since high Corisol reduces ACTH the adrenals degenerate and may cause hypo Aldo,...
ACTH does not have any effects on Aldo secretions.
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| mdwannabe
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no certainly not...but it has trophic effect upon the cortex in general. So once the cortex degenerates, Aldo is no where to be made.
Aldo is directly controlled by [K], and indirectly by [Na]
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| mjl1717
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First the Ca doesnt realy tell much in Cushings.
If anything as mdwannabe states(and hes one of the best physiologists I know) hypokalemia but not hypernatremia may be present
I think his statement makes BIG points:
1)Cortisol has weak mineralcortacoid activity so K decrease
2)Cortisol reduces ACTH therefore Adrenal cortex degenerates
causing hypoaldosteronism which counterbalances the K levels
The main 2 tests are Dexamethasone Suppression test and the 24 hr free
cortiol /creatinine ratio greater then 95ug
In working with mdwannabes hypothesis:
Just want to state [Cushings]
43%- pituatary adenama
10%-small cel lung CA
15%- due to a source that cant be located
32%- due to cortisol from the adrenals independent of ACTH
you can have adrenal cortex stimulation from totally exogenous sources
also!!
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| mani
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mdwannabe, r u sure that in the absence of ACTH there will be atrophy of zona reticularis as well?? can u share the source plz?
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| mdwannabe
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honestly, I don't know exactly the source, most likely I have made an inferrence from the some phisio facts. ACTH is necessary for the whole cortex to develop and function. ACTH has direct stimulatory effect upon Aldo. Exogenous glucorts diminish ACTH since it is controlled by cortisole. Hence, prolonged administration will "destroy" cortex, which we know happens. That will dimish all hormones produced, including sex, aldo and cort. However, we also know that in reality administration of glucs to pt, does not really cause hypoaldo. Unless we are talking about GRE (glucocorticoids remediable aldosteronism) there doses of glucs does lower abnormaly high aldo. Following that logic I have arrived at the above mentioned conclusions.
So here are the thoughts that have ran through my mind as I was typing the answer.
If any of it is wrong please let me know. Either facts or logic.
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| mdwannabe
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as far as text goes...I have studied Ganong and April, among some others available in my med school library. So what ever I know, or make impression of knowing, must have come from there.
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| mani
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i think it was mentioned somewhere in BRS physio that aldo is independant of ACTH. and the disorders in which ACTH is low there is no effect on aldo secretion
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| mdwannabe
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I don't know, I never read BRS, but look up in some other textbook. Also think about why are we so concerned about slowly withdrowing pt from steroids?
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| Kazem
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I remember that in Goljan Audio pathology,(in the topic of cellular injury) he says that in hypopituitarism when ACTH is low the middle and inner layers of adrenal cortex atrofies. the zona glumerolosa however that produces aldosterone is not affected.
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| vrach
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The following info is from my understanding of "Larsen: Williams Textbook of Endocrinology, 10th ed.,"-
-Cortisol and Aldosterone have very similar chemical stuctures. In the renal tubular cells Cortisol is metabolized to Cortisone (inactive) by the enzyme 11beta-hydroxysteroid dehydrogenase type 2, which is then excreted. This enables the binding of aldosterone to its receptor in the renal cell and exert its actions. When Cortisol is present in excess ammounts (Cushing's) or if the activity of this enzyme is compromised, Cortisol will bind to the Mineralocorticoid receptor and will exert the same effects as aldosterone (Cortisol is secreted in very large quantities, as compared to aldosterone, even in normal conditions).
-Elevated cortisol levels in Cushing's induces a negative Calcium balance, i.e, reduced intestinal Ca absorbtion, elevated renal Ca excretion-> calcicuria->elevated PTH.
-The effects of cortisol on osteoclasts is disputed.
-However, cortisol inhibits Osteoblast function->osteopenia, and osteoporosis.
-Bottom line: Blood Ca levels are unaffected, Calcicuria and kidney stones present, Hypokalemia, Na retention, Hypertension.
-ACTH does have a stimulatory effect on the zona glomerulosa, but it's absence in and of itself will not cause atrophy of this region. If the Renin-Anigiotnsin system is working normally, there will be no atrophy and the aldosterone levels will be normal, as in secondary hypocortisolism.
In cushing's, the hypertension caused by Cortisol will definetly suppress the Renin system also, causing hypotrophy of zona glomerulosa.
I would imagine that the extremly high levels of cortisol will always maintain Hypokalemia, even if aldosterone secretion is reduced!
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