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I'm not understanding the significance of the GnRH injection and subsequent LH increase. I assumed it was CAH and according to Uworld ACTH is given there, but that was wrong.
NBME 11 Question
- Thread starter Ronin786
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I'm not understanding the significance of the GnRH injection and subsequent LH increase. I assumed it was CAH and according to Uworld ACTH is given there, but that was wrong.
The girl in the question is evaluated for precocious puberty. Normal puberty is a function of hypothalamus-pituitary-gonadal axis, so you can start from there:
GnRH ---> LH, FSH ---> Sex hormones (E2, P, androgens)
The ultimate problem is the increase in sex hormones. Now this could be due to (a) Early maturation of the axis itself (called central precocious puberty) or (b) elevation of one of the component of the axis (e.g., use of exogenous estrogen [elevated E]).
The significance of GnRH injection is to differentiate between central and peripheral causes. If there's central precocious puberty, there will be an elevation of LH after GnRH injection; whereas in peripheral precocious puberty, there won't be an increase. This is because the level of sex hormone excess seen in central precocious puberty is high enough to initiate puberty, but not high enough to suppress LH secretion after GnRH injection.
Treatment of central precocious puberty is based on the etiology, but since most of the cases are idiopathic, I'll proceed like this is an idiopathic central precocious puberty case. Like I've said before, the problem in the central causes is the early maturation of the axis, where, like the normal puberty, pulsatile secretions of GnRH is seen. The goal of the treatment is to suppress this GnRH secretion. This is achieved by using GnRH analogues such as leuprolide. In a glance, this may seem contradictory, but continuous administration of GnRH analogues leads to downregulation of GnRH receptors in the pituitary gland. The end result is a steady state GnRH level, similar to the physiologic condition of a pre-pubertal child. This mechanism is also why GnRH analogues are used in the treatment of advanced prostate cancer.
GnRH ---> LH, FSH ---> Sex hormones (E2, P, androgens)
The ultimate problem is the increase in sex hormones. Now this could be due to (a) Early maturation of the axis itself (called central precocious puberty) or (b) elevation of one of the component of the axis (e.g., use of exogenous estrogen [elevated E]).
The significance of GnRH injection is to differentiate between central and peripheral causes. If there's central precocious puberty, there will be an elevation of LH after GnRH injection; whereas in peripheral precocious puberty, there won't be an increase. This is because the level of sex hormone excess seen in central precocious puberty is high enough to initiate puberty, but not high enough to suppress LH secretion after GnRH injection.
Treatment of central precocious puberty is based on the etiology, but since most of the cases are idiopathic, I'll proceed like this is an idiopathic central precocious puberty case. Like I've said before, the problem in the central causes is the early maturation of the axis, where, like the normal puberty, pulsatile secretions of GnRH is seen. The goal of the treatment is to suppress this GnRH secretion. This is achieved by using GnRH analogues such as leuprolide. In a glance, this may seem contradictory, but continuous administration of GnRH analogues leads to downregulation of GnRH receptors in the pituitary gland. The end result is a steady state GnRH level, similar to the physiologic condition of a pre-pubertal child. This mechanism is also why GnRH analogues are used in the treatment of advanced prostate cancer.