Congenital adrenal hyperplasia vs Addison's disease

[sbm1292987]

Hi everyone

If my understanding is correct, 17-hydroxylase deficiency presents with diminished secondary sexual characteristics due to reduced adrenal and gonadal synthesis of androstenedione and DHEA, which are precursors for testosterone and oestrogen. Is this correct, or are there different enzymes in the gonads and adrenal cortex? Also, does Addison's disease present with the same thing, because you get loss of androgen production? I imagine the gonads make enough to compensate, but I want to make sure.

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[ketosisevangelist]

The boards never test on how anyone learns it.


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[crazyboi1993]

I think CAH, the most common deficiency is 21-hydroxylase deficiency. Due to this enzyme deficiency, both cortisol and aldosterone synthesis are compromised, and the precursors are shunted to form androgens instead. This is the reason, why CAH presents with ambiguous genitilia, especially in females during birth, due to excess androgen production, b/c cortisol and aldosterone can't be formed, so the precursors build up and get shunted. Addison disease, I think is when there is aldosterone deficiency, so the patient will often go into Addison crisis, with hyponatremia and hyperkalima (if I could spell haha).

 

[TheBoneDoctah]

I think CAH, the most common deficiency is 21-hydroxylase deficiency. Due to this enzyme deficiency, both cortisol and aldosterone synthesis are compromised, and the precursors are shunted to form androgens instead. This is the reason, why CAH presents with ambiguous genitilia, especially in females during birth, due to excess androgen production, b/c cortisol and aldosterone can't be formed, so the precursors build up and get shunted. Addison disease, I think is when there is aldosterone deficiency, so the patient will often go into Addison crisis, with hyponatremia and hyperkalima (if I could spell haha).

You also don't have cortisol in Addison disease.


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