Lecture 23: Luteal phase and menstrual cycle Flashcards
What is the major steroid hormone produced?
P4
-Granulosa/theca cells luteinize and form C.L
-Steroid synthesis is truncated = progesterone is the final product
-Initially (fist few days), spontaneous granulosa cells form large luteal cells which lack LH receptors and autonomously produce ;are amounts of P4
-C.L remains independent of LH for ~6 days
-After this C.L becomes LH dependant which theca derived cells as predominant cells
-These start as small luteal cells, but differentiate to become large luteal cells and produce large amounts of P4
-Towards end of cycle most luteal cells are of the large type
SUMMARY
-After first few days after ovulation while CL reorganizes it self, the first ells to turn into progesterone producing cells are xgranulosa, spontaneously w/o help from anyone, produce target progesterone levels
-Several days later x theca cells (that have LH receptors under influence of LH) will also transform themselves into luteal cells initial small but gradually become large cells, and become predominant cell mass of CL producing progesterone
What is the endometrium cycle? What are the 3 phases?
-Development of the endometrium is timed with cyclic changes in estradiol and progesterone
Phase 1: Proliferation phase
-During follicular growth phase, estradiol stimulates growth of stratum functionalis (increase cell #s and thickness)
Phase2: Secretory phase:
-During luteal phase, progesterone stimulates development of uterine gland (where embryo makes contact)
Phase3: Menstral phase
-Decrease in ovarian steroid induces the necrosis of stratum functionalis (if nothing happens P4 decrease and again switch to Increase Estrodiol shut off blood supply and shed superficial layer of endometrium)
What happens at the level of the cells/tissues of the proliferative phase?
-Endometrium is divided into 2 layers (basal, functional)
-Glands are straight and narrow throughout the entire length
-Glandular epithelial starts to multiply
-Spiral arteries system develops in the functionale (invasive network of capillaries to support fetus)
-Basal layer always there where endocrine regenerates from after menstruation
What happens in the secretory phase?
-Glands are more tortuous (channels, side channels instead of straight)
-Spiral arteries extend to the epithelial layer
-Glandular epithelium loaded with glycogen (supply fetus with all nutrients as well as O2)
What happens in the menstrual phase?
-If nothing happens tell ovary sorry no embryo CL will destroyed, and levels of P4 decreases, that will shut off blood supply to functional layer of endometrium
-Functional layer regresses, shrinks and atrophies
-Super coiling of spiral arteries
-Reduced blood flow= release of toxic and vasoactive substances (twist, block blood supply snow ball effect tissues dies and signal further triggers apoptosis)
-Vasoactive substances= physiological endometrium “infraction” (terminate blood supply and that part of body is dying)
What are the hormones involved?
Form follicles
-Estradiol released during follicular phase
-ERalpha in endometrium= mitosis
-Progesterone during the luteal phase inhibits mitosis, stimulates mucus secretion from uterine glands and reflexes smooth muscle
From uterus
-Prostaglandins: local effect
-PGF2Alpha constricts uterine arterioles=anoxia
-Endometrium sloughed=menses start
Where do prostaglandins travel?
-They have a short half-life so PGF2alpha travels from utero-ovarian vein to the ovarian artery
What are prostaglandins?
-Defined from liposoluble membrane lipids, why they are able to dice so easily from uterine vein to ovarian artery
What is the influence of the ovary and the CL and the communication b/w the 2?
- Message triggering loeutiallysis is coming from the uterus
- Coming mostly form the same side, makes sense bc uterine vein on each side so if remove uterus on that same side removing source of PGF2alpha but still come from other side but not enough to still delayed
What are the actions of exogenous PGF2apha on luteal cells?
Large cells
-PGF2a receptors (after 5d)
-Produce 80-90% of total progesterone synthesis
-Contain oxytocin as cytoplasmic granules
Small cells
-LH receptors
-injections of PGF2a after d5 are luteolytic
-Reduce blood flow to CL
-PGF2a binds to receptors on large cells to (release oxytocin by endocytosis, and inhibit conversion of cholesterol tp pregnenolone)
-collateral loss of small cells (days)
-Cellular degeneration (days)
