Final answer:
In 17 alpha hydroxylase deficiency, there is an increase in mineralocorticoids such as 11-deoxycorticosterone (DOC) and corticoosterone, leading to symptoms of mineralocorticoid excess. This condition arises from a genetic defect that impedes the production of glucocorticoids and sex steroids, causing a buildup of precursor hormones in the mineralocorticoid pathway.
Step-by-step explanation:
In 17 alpha hydroxylase deficiency, there is an increase in mineralocorticoids such as 11-deoxycorticosterone (DOC) and corticoosterone, which can lead to symptoms of mineralocorticoid excess like hypertension and hypokalemia. This condition is due to a genetic defect in the enzyme 17 alpha hydroxylase, which is essential for the production of cortisol and sex steroids. Without the enzyme's activity, there is a shunting of precursors toward the mineralocorticoid pathway, hence the increase in mineralocorticoids.
17 alpha hydroxylase deficiency also results in decreased production of glucocorticoids (cortisol) and sex steroids (androgens and estrogens). Due to the lack of cortisol, there is increased secretion of adrenocorticotropic hormone (ACTH) from the pituitary gland, which fails to increase cortisol levels but furthers the production of mineralocorticoids.