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Discussion Starter · #1 ·
In Pathoma, it says that Cushing's leads to HTN with hypokalemia and metabolic acidosis. (In that section is says there's an increase in alpha-1 rec --> vasoconstriction and that at very high levels, cortisol stimulates mineralcorticoid receptors, but aldo stays normal.)

In my mind, there should be a metabolic alkalosis if your have hypokalemia via mineralcorticoid receptor stimulation.

Is this a misprint by chance? Or is there some other explanation? Hussain just ignores the metabolic acidosis on the slide and doesn't explain it.
 

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They are all steroid except Aldo

High glucocorticoids in the blood over whelm the enzyme responsible to inactivate them to act as mineralocorticoids
Normally
Cortisol cant act as mineralocorticoids because it is converted to cortisone

When cortisole is high
it can preform it's
mineralocorticoidsaction effect by attaching to the same receptor as aldosterone and it has more affinity to it (they are all come frome the cortex; have similarities in the structure)
Hope that's helping you

 

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Discussion Starter · #3 ·
Metabolic Acidosis

High glucocorticoids in the blood over whelm the enzyme responsible to inactivate them to act as mineralocorticoids
Normally
Cortisol cant act as mineralocorticoids because it is converted to cortisone

When cortisole is high
it can preform it's
mineralocorticoidsaction effect by attaching to the same receptor as aldosterone and it has more affinity to it (they are all come frome the cortex; have similarities in the structure)
Hope that's helping you

I still don't understand where the metabolic acidosis is coming from though. If it acts like Aldo, it should produce hypokalemia and metabolic alkalosis.
 
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