According to FIGO manual (1990) causes are: Tubal and peritoneal factors (25–35%), Ovulatory factor (30–40%) and Endometriosis (1–10%).
Ovarian factors: The ovulatory dysfunctions (dysovulatory) encompass:
- Anovulation or oligo-ovulation
- Decreased ovarian reserve.
- Luteal phase defect (LPD)
- Luteinized unruptured follicle (LUF).
ANOVULATION OR OLIGO-OVULATION
The ovarian activity is totally dependent on the gonadotropins and the normal secretion of gonadotropins depends on the pulsatile release of GnRH from hypothalamus. As such, ovarian dysfunction is likely to be linked with disturbed hypothalamo-pituitary-ovarian axis either primary or secondary from thyroid or adrenal dysfunction.
Thus, the disturbance may result not only in anovulation but may also produce oligomenorrhea or even amenorrhea. Anovulatory cycles usually represent a lesser degree of disturbance with these normal pathways than does amenorrhea. As there is no ovulation, there is no corpus luteum formation. In the absence of progesterone, there is no secretory endometrium in the second half of the cycle. The other features of ovulation (later in the chapter) are absent.
LUTEAL PHASE DEFECT (LPD)
In this condition, there is inadequate growth and function of the corpus luteum. There is inadequate progesterone secretion. The lifespan of corpus luteum is shortened to less than 10 days. As a result, there is inadequate secretory changes in the endometrium which hinder implantation. LPD is due to defective folliculogenesis which again may be due to varied reasons. Drug induced ovulation, decreased level of FSH and/or LH, elevated prolactin, subclinical hypothyroidism, older women, pelvic endometriosis, dysfunctional uterine bleeding are the important causes.
The medicines that can be thought of use are:-