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Difficulty: EasyReproductive Endocrinology and Infertility

Match each etiology of secondary amenorrhea with its characteristic endocrine laboratory profile.

  • Primary ovarian insufficiencyHigh FSH, high LH, low estradiol
  • Functional hypothalamic amenorrheaLow or inappropriately normal FSH and LH, low estradiol
  • Polycystic ovary syndromeHigh LH/FSH ratio, high testosterone, normal or high estradiol
  • ProlactinomaHigh prolactin, low FSH and LH, low estradiol

Answer

Primary ovarian insufficiency is paired with high FSH/LH and low estradiol. Functional hypothalamic amenorrhea is paired with low FSH/LH and low estradiol. Polycystic ovary syndrome is paired with a high LH/FSH ratio and high testosterone. Prolactinoma is paired with high prolactin and low FSH/LH.
Each etiology has a distinct pathophysiologic mechanism that dictates its laboratory profile. Primary ovarian insufficiency is a primary gonadal failure (hypergonadotropic hypogonadism). Functional hypothalamic amenorrhea and prolactinomas cause central suppression of GnRH (hypogonadotropic hypogonadism), with prolactinoma specifically showing elevated prolactin. PCOS causes an imbalance in gonadotropins (high LH) with excess androgen production.

Step-by-Step Solution

1
Analyze the laboratory profile of primary ovarian insufficiency.
Identified as hypergonadotropic hypogonadism (High FSH, high LH, low estradiol).
The primary defect is at the level of the ovary, resulting in absent estrogen production and thereby removing negative feedback on the pituitary.
2
Analyze the laboratory profile of functional hypothalamic amenorrhea.
Identified as hypogonadotropic hypogonadism (Low/normal FSH and LH, low estradiol).
The primary defect is a decrease in pulsatile GnRH secretion from the hypothalamus, leading to decreased pituitary gonadotropins and subsequent low ovarian estrogen.
3
Analyze the laboratory profile of polycystic ovary syndrome.
Identified as a normogonadotropic normoestrogenic state with hyperandrogenism (High LH/FSH ratio, high testosterone).
Altered GnRH pulsatility increases LH over FSH, stimulating ovarian theca cells to produce excess androgens.
4
Analyze the laboratory profile of a prolactinoma.
Identified as hyperprolactinemia causing hypogonadotropic hypogonadism.
Excess prolactin inhibits GnRH secretion, leading to decreased FSH and LH, and consequently low estradiol.

Key Concept

Endocrine laboratory profiles in secondary amenorrhea
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Topics

Reproductive Endocrinology and Infertility

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