babydoc4usmle
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hey, SMART DUDES ; )
i have a Q
when we have deficiency in 17 alfa-OH, we get increas in 11-DOC synthesis --> incr ECF, incr BP, incr Na --> decr renin and AT-II --> decr aldo
but if we decr AT-II we decrease conversion of cholesterole to pregnenolone because desmolase (converting enzyme) is stimulated by AT-II...
decr AT-II --> decr pathway downstream --> decr 11-DOC
is it ACTH that still stimulates desmolase? or there is other mechanism?
please, explain
thanks : )
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| Ancylostoma
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Topics: 42
Posts: 642
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If you have the kaplan physiology notes the best explanation comes from the diagram with the enzymes. The lack of 17 alpha hydroxylase causes the increase or pathway that produces 11-doc and what you have said is therefore correct. the lack of production of cortisol, prevents the normal feedback inhibition and thus elevates the amount of acth. acth stimulates the conversion of cholesterol to pregnenolone by desmolase. So basically you were right.
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| babydoc4usmle
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ahaaaaaaaaaaaaaaaaaaa.........so, incr ACTH wants to secret cortisol (via ZF pathway), but since we don't have converting enzyme from ZG to ZF we get excess in ZG pathway until 11-DOC, which will not get coverted to Aldo due to insuff in AT-II....right?
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| babydoc4usmle
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Topics: 18
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but there is a slight inconsistency...ACTH controls ZF' cortisol, AT-II controls aldo....and K notes confirm it.....hmmm......
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| Ancylostoma
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Topics: 42
Posts: 642
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right, but since there is no 17 a oh, the only thing that is left in the ZF, is the enzymes to create pregnenelone, and then continue on like it was the ZG because all the other enzymes are present. I dont know, thats my understanding but the logic works in answering the questions so I have stuck with it.
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| babydoc4usmle
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Topics: 18
Posts: 634
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ic..thanx
; )
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