Luckyall
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Give it a shot , guys, is all worth it !
And more and more important, enjoy it 
Whas the mechanism of HTN in a pt with 11 hydroxylase deficiency enzyme ?
A) decr Cortisol
B) incr. 11 DeoxyCorticosterone release in circulation from Zona fasciculata , reticularis and z. glomerulosa
C)only an incr 11 Deoxy corticosteron release in circulation from Z. fasciculata reticularis
D) only an incr. in 11 Deoxy Corticosterone release in circulation from z. glomerulosa
E) an incr. in angiotensin II
F ) A decr in A II
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| RayBerg
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I'd say D!?
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| silver
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D
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| Luckyall
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 , in fact thas why i posted this particular Qs
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| silver
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Luckyall wrote:, in fact thas why i posted this particular Qs
didn't get u, what r u trying to say?
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| Luckyall
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answer is actually C zona glomerulosa doesnt release into circulation 11DOC( DEOXY CORTICOSTERONE), this is not a normal output . In 11 hydrox. defic---> look a 2 aspects
1) Z glomerulosa --> decr Aldosterone
2) Z fascic, reticularis---->decr Cortiso, &decr Androgens. From decr Cortisol---> incr ACTh---> incr products before the blockade, a clinical significant one is incr 11DOC (wich is a normal minor output in this Z. fascic-reticularis) ----> the only one responsible for HTN.
So is incr 11DOC from Z fascic , reticul---> HTN and NOT incr 11DOC in Z glomerulosa wich is not even a Normal output released into circulation of the Z glomerulosa
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| silver
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you're question is asking about 11-hydroxylase deficiency.
it's clearly written in kaplan that 11-hydroxylase def. would lead to accumalation of 11-deoxycorticosterone which is ONLY produced in z.glomerulosa and can cause an increase in blood pressure, due to its mineralocorticoid property.
if 11-hydroxylase is deficient in z.fasciculata it would lead to accumalation of 11-deoxycortisol which is a glucocorticoid having NO EFFECT ON BLOOD PRESSURE.
mineralocorticoid activity is ONLY in z.glom. and not in z. fasciculata
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| Luckyall
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Well look in Kaplan... is a very BIG & common confusion.
The only CIRCULATORY output of Z glomer---> aldosterone, and in 11 hydrox defic you only have deficient Aldosterone. The incr 11 DOC from Z glomerulosa will NOT be released in circ---> therefore NOt leading to HTN.
But 11 DOC is one NORMAL minore CIRCULATORYoutput of Z fasciculata, reticularis , and in a 11 DOC defic----> this 11 DOC circulatory output ( wich normally is monor) INCREASES----> is THIS 11 DOC from Z fascic, reticularis that is responsible for HTN.
Read it again , plz, Kapl. explains it wonderful!
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| silver
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Luckyall wrote:
The incr 11 DOC from Z glomerulosa will NOT be released in circ---> therefore NOt leading to HTN.
what's your reference for this plz?? where did you read this??
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| silver
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Luckyall wrote:
But 11 DOC is one NORMAL minore CIRCULATORYoutput of Z fasciculata, reticularis
which flow diagram in kaplan is showing you that 11-deoxycorticosterone is being produced in z.fasciculata and z. reticularis????
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| Luckyall
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 Kaplan, physio ! Go back to it... reread it till you get it , is the most common mistake !!!
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| silver
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what's the page number and where is the EXACT line??
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| silver
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11-DOC is produced ONLY in z.glomerulosa and it's written in plain english that it is responsible for Na+ retention thereby increasing blood pressure. (written right above fig. IX-3-9).
whereas, it is not mentioned anywhere in kaplan endo. that 11-DOC is released from z.fasciculata or reticularis.
if you still think it is, show me the exact page and line
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| silver
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here's the kaplan we're all studying from, don't know about you.........
Attached Files:
11 - Hydroxylase Deficiency.doc (251 KB, 13 downloads)
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| RayBerg
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Lucky, I, too, derived that answer based on Kaplan and Dr Dunn's lectures.
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| Luckyall
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common, guys, listen to Dunn !!!
pg 387-388 kaplan CLEARLY mentions the Normal hormonal outputs,do read that....
Then listen to Dunn's lectures... after that come and post whas that all about .
Edited by Luckyall on 05/27/07 - 11:35 AM
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| keepgoing
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even check dr goljan's systemic path in endo part...i agree with luckyall,very interesting concept and liked it.
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| me007
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according to Goljan's diagram, there is no deoxycoticosterone produced in reticularis (which is the last option in C)
and there is a deoxycortisol , not deoxycorticosterone produced in z. fasciculata.
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| Addicudo
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D) only an incr. in 11 Deoxy Corticosterone release in circulation from z. glomerulosa
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| epica
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Ans is D
FA page 263, also Kaplan.
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| epica
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Lucky are u agree?
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| Luckyall
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nope.. do listen to Dunn's physiol. lectures ...
Answer to this Qs is C... do read above
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| Luckyall
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if any blockage on zona glomerulosa----> the ONLY thing that we can see in here is decr Aldosterone and its lacking effects, thas it !!! 11 DOC is not a normal output of Z glomerulsa... therefore is not released into circulation from Z glomerulasa under NO circumstances !!!
BUT if you look up Kaplan , i quoate pg above.... 11DOC is a minor output of Z retic-fascic under NORMAL CONDITIONS. If 11 hydroxylase def enzyme thgis output is not minor anymore.. is MAJOR and it is released in circulation from Z glom retic---> its effects in circulation ---> HTN
I hate this subject already... if anything , Kaplan and Dunn's lectures are saying it
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| Idlehands
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we're only trying to clear our concepts, why r u getting aggravated, luckyall
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| Idlehands
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Its not that we r not getting ur point but actually have told us something new which we didnt know so sorry for being clumsy n lazy it will take us time to get it through and u know most of us kinda like to read it with our own eyes n then understand the concept
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