Pathology- Congenital Adrenal Hyperplasias Autosomal recessive defect in enzymes related to the production of cortical steroids. Bilateral nodular hyperplasia of the adrenal gland with lipid-depleted cortical cells. 21-beta-hydroxylase deficiency disrupts the production of aldosterone and cortisol, leading to the redirection of precursor molecules to produce sex hormones. 11-beta-hydroxylase deficiency disrupts the production of aldosterone and cortisol, leading to the redirection of precursor molecules to produce sex hormones. 17 alpha-Hydroxylase deficiency disrupts the production of cortisol and sex hormones, leading to the redirection of precursor molecules to produce aldosterone. 21-beta Hydroxylase deficiency presents with masculinization, hypotension, hyperkalemia, and hyponatremia, which can result in hypovolemia due to salt wasting. 11-beta Hydroxylase deficiency presents with masculinization, premature puberty, hypertension (caused by the weak mineralocorticoid activity of 11 beta deoxycorticosterone), and no salt wasting. 17-alpha Hydroxylase deficiency presents with hypertension, hypokalemia, lack of sexual development, and low cortisol levels. Administering hormones to correct deficiencies and providing treatment for symptoms.
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