Etiology about 85% of all duB In adolescents Immaturity of the hypothalamic-pituitary-ovarian axis Especially, low response of hypothalamus and pituitary gland to positive feedback from estrogen In transitional period to menopause (premenopausal/premenopausal) ow response of the remaining follicles to gonadotropins Women of reproductive age Stress. fear etc. interferes with ovulation
Etiology • About 85% of all DUB • In adolescents Immaturity of the hypothalamic-pituitary-ovarian axis. Especially, low response of hypothalamus and pituitary gland to positive feedback from estrogen. • In transitional period to menopause (premenopausal/premenopausal) Low response of the remaining follicles to gonadotropins. • Women of reproductive age Stress, fear, etc. interferes with ovulation
Pathophysiology 1. Patterns of bleeding Withdrawal bleeding Decrease in estrogen Breakthrough bleeding Low level of estrogen High level of estrogen
1. Patterns of bleeding • Withdrawal bleeding Decrease in estrogen • Breakthrough bleeding Low level of estrogen High level of estrogen Pathophysiology
2. Mechanism of the bleeding Lack of progesterone causes defects in the self- limiting mechanism of menstruation 1) Friability of tissue Lack of stromal support 2)Incomplete shedding of endometrium Not enough stimulation for epithelial regeneration ( Complete loss of tissue is an effective stimulant for epithelial regeneration
2. Mechanism of the bleeding Lack of progesterone causes defects in the selflimiting mechanism of menstruation 1) Friability of tissue Lack of stromal support. 2) Incomplete shedding of endometrium Not enough stimulation for epithelial regeneration. (Complete loss of tissue is an effective stimulant for epithelial regeneration.)
3)Abnormal structure and function of blood vessels Lack of spiralization of the arteries 4)Abnormal production of vascular factors pGE,T. PGL i causing dilation of blood vessels (Proliferative endometrium produces PGE2) 5)Abnormal coagulation and Fibrinolysis Defects in tf and pal-i
3) Abnormal structure and function of blood vessels Lack of spiralization of the arteries. 4) Abnormal production of vascular factors PGE2, PGI2 causing dilation of blood vessels. (Proliferative endometrium produces PGE2) 5) Abnormal coagulation and Fibrinolysis Defects in TF and PAI-I
Pathologic changes of endometrium Hyperplasia endometrium Simple hyperplasia Complex hyperplasia Atypical hyperplasia 2) Proliferative phase of endometrium 3) Atrophic endometrium
3. Pathologic changes of endometrium 1) Hyperplasia endometrium • Simple hyperplasia • Complex hyperplasia • Atypical hyperplasia 2) Proliferative phase of endometrium 3) Atrophic endometrium