Dear Sabio,
well thanks for the linked references. good references.
however, i wasnt wrong about the 11-deoxycorticosterone having its effects in the z.fasciculata. yes it should be read primarily as in z.glomerulosa, but let me ask u, how do u get 11-deoxycortisol in the z.fascilulata? from progesterone in z.glomerulosa rite? its all interlinked. like when u have 11-beta OH deficiency how several pathways are affected. anyways, if u have the kaplan notes u can look up cushing syndrome. these are the characteristics listed for hypercortisolism (cushing syndrome):
1. protein depletion as a result of excessive protein catabolism
2. inhibition of inflammatory response n poor wound healing
3. hyperglycemia leads to hyperinsulinemia and insulin resistance
4. hyperlipidemia
5. bone dissolution and osteoporosis
6. thinning of skin with purple striae around abdomen
7. increased adrenal androgens (from zona reticularis!!)
8. MINERALOCORTICOID effects of the high levels of glucocorticoid leading to salt and water retention, hence potassium depletion and HYPOKALEMIC alkalosis.
9. redistribution of body fat
well, this is what i got from the KAPLAN notes and guyton physiology. i guess as info provided by sabio, if we wanna update ourselves then we should read his articles. but then for our exam, dont we need to clearly understand for now, that our references points towards an explanation of the hypokalemia and increase in mineralocorticoids indirectly in cushing disease? or should we stick to thinking that what happens in each zone does not affect the others? how? how? how?
