Reproductive Physiology PDF

Reproductive Physiology Sex Determination and Differentiation Lecture 1 Puberty and Reproductive Capacity Male Reproductive Tract Function Lecture 2 Female Reproductive Tract Function Lecture 3 Pregnancy, Parturition, Lactation...

Reproductive Physiology Sex Determination and Differentiation Lecture 1 Puberty and Reproductive Capacity Male Reproductive Tract Function Lecture 2 Female Reproductive Tract Function Lecture 3 Pregnancy, Parturition, Lactation 1  Reproductive Physiology Lecture 2-1 Female Reproductive Tract Function Overview of oogenesis Hormonal control of oogenesis Process of oogenesis Ovarian phases of the menstrual cycle 2  2-1 A Overview of female structures and process of oogenesis This video is a clip from the longer original video. It will end somewhat abruptly at slide 9 3 Female Reproductive System- Side view Fig. 17.13a 4 Figure 17-17: Female Reproductive System: front view 5  Oogenesis. Fig. 17.19 (within the ovary) 46 chromosomes, 1 chromatid/chromosome poolofprecursorcells At ~ 7 months t.ee gestation- DNA replicated , then 46 chromosomes, meiotic arrest 2 chromatids/chromosome 2-4 million primary oocytes available at birth 1 oocyte per Tiles DEGENIEATION cycle completes 200,000-400,000 primary oocytes available at puberty 1st meitoic division 23 chromosomes, 2 chromatids/chromosome 23 chromosomes, ~400 secondary oocytes ovulated EETEYT.FIiiEattion 1 chromatid/chromosome 6 between puberty and menopause 2ndmeffictivisionoccurswhenfertilizationoccurs  Fig. 17.1 n chromosomes in ovum nucleus Gametogenesis (Oogenesis) in females + n chromosomes in sperm nucleus making a new ovum viablecell Nuclei fuse ovulated nx2 Produced from oogonia by mitosis and start of meiosis during fetal development at 7monthsgestation Fertilization causes meiosis II n Non-viable cell 2nx2 onlyiffertilizationoccurs does the secondmeiotic occur divison LH Surge of menstrual cycle restarts meiosis I nx2 non-viable cell 7  Figure 17-20 If no FSH, LH; these follicles undergo “atresia” = degradation Progression to early antral expleptots stage does NOT require FSH and LH, expressFSHreceptors therefore it can Ocythaggnulosacells occur through LH receptors infancy and on early antral childhood, and theca cells also during the fromtheca testosterone menstrual FSH receptors cells diffusestogranulosa 8nbkgggmoatgfg.ge'ments cycle. on early antral granulosa After puberty, Tespondto cells during each cycle, Jen's FdFdd 10-25 pre- and early antral follicles begin to develop further due to increased FSH and 8 Only 1 Dominant (mature) follicle forms each cycle LH continuedmaturationoffollicle  Figure 17.23 Ovarian Estrogen Secretion after puberty GnRH pulses (Hypothalamus) (From anterior pituitary) (From anterior pituitary) (testosterone) Granulosa cells contain the enzyme aromatase Early follicular phase, granulosa cells express FSH receptors only. Late follicular phase granulosa cells of dominant follicle begin to express LH receptors as well. 9 2-1B is a clip from the longer original video. It will start without much intro at slide 11. Break in Lecture 2-1 2-1 B follows Hormonal control of oogenesis Process of oogenesis Ovarian phases of the menstrual cycle 10  Fig 17-21. Menstrual Cycle Ovarian phases cellsareexpressingdiff enzymestomake morepro 1914896,9 thanestrogen gesterone theonefollicle 2o oocyte released 1o oocyte(s) containsa 1 oocyte 11  Fig 17.22. Hormonal Changes and Ovarian Events during Menstrual cycle These are daily averages, and do not reflect pulses within a given day Anterior pituitary Note different scales Ovary Inhibin (not shown) o Release pattern similar to estrogen 12 Fig. 17.22 Bigging Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.  Figure 17.22 Early Follicular Phase: Day1 5 1. LH and FSH increase 2. Multiple follicles mature past early antral stage 3. As estrogen rises slightly, it exerts negative feedback. Inhibin is secreted from arevery Progesterone estrogen low granulosa and exerts negative andthatremovestheinhibition feedback on FSH EHEQBg.infoinEreha'seasaresult Mid-Follicular Phase As estrogen (and inhibin) 4. Dominant follicle “selected” increases, FSH decreases. (probably has granulosa cells Only one follicle typically is with the most FSH receptors sensitive enough to survive and beginning to express LH the decrease in FSH = receptors) dominant follicle Thisstimulatestheselectionofthe 5. LH and FSH + highly sensitive dominantfollicle dominant follicle increased developbut Multiplefollicles thereis onlyONE thatismatureenough has estrogen and inhibin secretion enough FSH receptorsto to continue respondasFSHlevels decrease 6. FSH levels fall, causing non- Asestrogenbeginsto increaseFSHbegins dominant follicles to undergo todropTypically onefollicle only that survives atresia fE.infogEnto.uicieisnowreleasingaiot 13 Early-Mid Follicular Phase Fig 17.24 Estradiol (estrogen) feedback inhibits amplitude of GnRH pulses GnRH ~1 pulse/hr Estradiol (estrogen) both feedback inhibits amount of FSH and LH released in Granulosa cells response to a given amount Have only FSH receptors of GnRH from early until mid follicular phase Frittianif FSH increases aromatase Aromatase converts Theca cells androgens from theca cells Have only LH receptors to estrogens LH promotes Estrogen increases # of FSH conversion of receptors becomesmoreresponsive cholesterol  FSH increases inhibin androgens (primarily Inhibin decreases FSH testosterone) Around mid-follicular phase, LH receptors start to appear 14 on dominant follicle  Figure 17.22 Mid-Late Follicular Phase 6. Dominant follicle only. domain Other follicles are undergoing 8 8regarduces atresia 7. Many theca so lots of testosterone, and many granulosa cells are converting the *LH surge 1. Progesterone testosterone to estrogen production begins 2. Estrogen production 8. High estrogen has a dips STIMULATORY effect on 3. Meiosis 1 occurs 4. Enzymes activated to GnRH pulses and LH digest follicle wall secretion (effects are at 5. 2o oocyte is ovulated hypothalamus and anterior 6. Remaining follicular cells changed into pituitary) POSITIVEFEEDBACKmassive luteal cells (corpus increasein H 9. End of follicular phase: luteum forms) F LH surge* 10. 1 meiotic division, st ovulation, corpus luteum formation 15  Fig. 17.25 Mid-Late follicular Phase & Ovulation LH surge triggers: Changes within follicle o Oocyte completes 1st meiotic division, is now 2o oocyte o Estradiol synthesis drops o Progesterone synthesis starts Corpus Luteum Ovulation (~18 h after peak of Can do full LH surge) ovulationoccurs peakofsurge synthesis pathway cholesterol  o Activation of enzymes that progesterone  break down walls of follicle testosterone  and ovary estradiol o Release of 2o oocyte surrounded by cumulus Luteinization o Transformation of follicle into corpus luteum follicle o Converts granulosa cells into large luteal cells and theca to small luteal cells o Large increase in 2o oocyte swept progesterone secretion into fallopian tube by fimbriae Estrogen peaks ~1 day before LH surge and inhibin 16 Ovulation 2 oocyte li 17 IMAGES IN REPRODUCTIVE MEDICINE Laparoscopic observation of spontaneous human ovulation Jean-Christophe Lousse, M.D., and Jacques Donnez, M.D., Ph.D. Department of Gynecology, Universite Catholique de Louvain, 1200 Brussels, Belgium We report laparoscopic observation of spontaneous human ovulation, illustrated by protrusion of the mature follicle and oocyte release into the peritoneal cavity. (Fertil Steril 2008;90:833–4. 2008 by American Society for Reproductive Medicine.) FIGURE 1 18 Figure 17.22 Luteal Phase 11. Corpus luteum forms duetoLHsurge 12. Progesterone and estrogen at high levels (inhibin also secreted) 13. Progesterone, with estrogen’s “help”, inhibits GnRH and LH. Inhibin inhibits FSH 14. Lasts about 14 days LH is falling throughout 15. If no fertilization, corpus luteum starts degenerating around d25 decreased progesterone and estrogen, which then 16. FSH and LH start to rise, menstruation will begin = cycle is over and new cycle is beginning menstruationbeginswhen 19 progesterone estrogenAND FSH LH  g Luteal phase. Fig 17-26 Progesterone inhibits the frequency of GnRH pulses GnRH ~1 pulse every 4 hrs Progesterone prevents another LH surge despite high estrogen estrogen helps with inhibition because it stimulates production of progesterone receptors, thereby increasing progesterone’s inhibitory effect Though decreasing throughout, the LH & FSH levels are high enough to maintain the corpus luteum for ~14 days 20 Corpus Luteum 21  Hormone Changes and Ovarian Events during Menstrual Cycle 1. Bleeding begins. Low estrogen levels, so FSH and LH secretion increases. FIRST DAY OF NEW CYCLE! 2. 10-25 pre and early antral follicle develop further due to FSH and LH increase 3. For ~1 week: FSH stimulates granulosa cells, LH stimulates theca cells. Theca cells proliferate & synthesize androgens. Granulosa cells proliferate, increase aromatase activity, & convert androgen to estrogen. Estrogen levels begin to rise slowly. 1. Rising estrogen  GnRH inhibition  FSH levels decrease 2. Rising inhibin FSH levels decrease due to effects at anterior pituitary 3. Rising estrogen LH levels stabilize due GnRH inhibition and due to effects at anterior pituitary 4. One follicle becomes dominant, likely because its granulosa cells are more sensitive to FSH and have gained receptors for LH. All other developing follicles undergo atresia because of the decreasing FSH and stabilized LH secretion. 5. Estrogen levels increase more as granulosa (and theca cells) in dominant follicle proliferate 1. Increased testosterone production by theca cells and increased aromatase activity increased estrogen 6. FSH levels drop more than LH because inhibin specifically inhibits FSH beyond estrogen’s effects via GnRH 7. High estrogen levels begin to exhibit positive feedback and 22 8. LH surge occurs (it’s the stimulus that triggers #’s 9, 10 and 11…next slide)  Hormone Changes and Ovarian Events during Menstrual Cycle 9. LH surge triggers: 1o oocyte completes first meiotic division- now have a 2o oocyte 10. LH surge triggers: Ovulation: 1. Granulosa cells decrease estrogen and increase progesterone secretion 2. Enzymes and prostaglandins from granulosa cells break down follicular-ovarian membrane and the weakened membranes rupture 3. 2o oocyte and surrounding granulosa cells (cumulus) are released 11. LH surge triggers: Corpus luteum development from the remaining dominant follicle cells within the ovary. 12. High levels of progesterone and estrogen are secreted by the corpus luteum plasma levels increase (inhibin is also secreted) 13. GnRH and LH secretion directly inhibited by progesterone (especially in the presence of estrogen). FSH is directly inhibited by inhibin and indirectly by progesterone+estrogen) 14. Corpus luteum has life-span of 14 days unless fertilization occurs 15. No fertilization degeneration of corpus luteum progesterone and estrogen levels decrease, freeing FSH and LH from inhibition 16. Bleeding begins as FSH and LH levels rise…new cycle begins 23 Figure 17-1 Summary Hormonal Control of Female Reproduction Early to mid follicular phase: + FSH and LH rise due to low estrogen and progesterone Multiple follicles developing Pulsatile As follicles develop, estrogen slowly Secretion increases and is inhibitory at hypothalamus (GnRH) and anterior pituitary (LH directly and FSH via GnRH) As follicles develop, inhibin is produced by granulosa cells and inhibits FSH from anterior pituitary Mid to late follicular phase: 1 dominant follicle estrogen levels increase dramatically, but still inhibitory Late follicular phase: Very high estrogen is stimulatory to GnRH, FSH and LH LH surge At varying points, FSH levels do not increase as much as LH because of inhibin estrogen, inhibin, Luteal phase progesterone Progesterone + estrogen inhibit GnRH and LH; inhibin and decreased GnRH inhibit FSH 24  Remember the hypothalamus! Relative GnRH pulse frequency and amplitude Amplitude and frequency increase Amplitude Frequency decreases decreasing Hypothalamus Pituitary Ovary inhibin 25 Slide adapted from Dr. Suzanne Moenter  Review Ovarian follicles house primary oocytes – Primary oocytes have 2nx2 chromosomes and are in meiotic arrest – Follicles develop in waves of about 10-25 at a time – If FSH and LH too low (i.e., pre-puberty, or during mid-follicular phase)  atresia occurs at preantral-early antral phase Each cycle, usually only one follicle is able to continue maturing past mid-follicular phase when negative feedback by estrogen (on GnRH and LH) and inhibin (on FSH) cause the FSH and LH levels to begin to decrease – The one dominant follicle secretes high levels of estrogen that, at the end of follicular phase, become stimulatory to GnRH (and so to LH and FSH) – All other developing follicles undergo atresia prior to the LH surge Ovulation (end of follicular phase) – High estrogen LH surge 1st meiotic division, ovulation of secondary oocyte (nx2 chromosomes) and corpus luteum formation 26  What you should have learned (2-1 A and B): Basic anatomy of female tract Process of Oogenesis Hormonal control of menstrual cycle: GnRH, LH, FSH, testosterone, estrogen, progesterone, inhibin Functions of granulosa cells and theca cells Menstrual cycle – Hormonal changes – Ovarian changes (Follicular phase and Luteal phase) LH surge and ovulation Apply information to solve problems 27  Reproductive Physiology Lecture 2-2 Female Reproductive Tract Function Uterine phases of the menstrual cycle Hormonal control of uterine phases Hormonal contraception (female) Menopause 28  2-2A slides 30-36 Uterine Phases of the menstrual cycle This is a shorter clip from the longer original video. 29  What’s going on in the uterus during the ovarian follicular and luteal phases? Follicular phase (ovary) coincides with Menstrual and Proliferative phases (uterus) Luteal phase (ovary) coincides with the Secretory phase (uterus) 30 Uterine changes are caused by cyclical changes in ovarian hormones. Fig 17.27 Proliferative phase: increasing estrogen Growth of endometrium & 2o oocyte (memory tip: progesterone is myometrium (uterine “pro-gestation”) smooth muscle) Synthesis of progesterone end duringsecretoryphasethe metriumbeginstosecret substan receptors in endometrium tosupportImplantationOta fertilizedegg Endometrium: endometrium itsstimul loses epithelial lining ae fit Tatanka cycle attn of the uterus nnerepithelialcelllayer Myometrium: smooth muscle layers of uterus muscle mooth layer B Effing phaseestrogenlevelslow follicular Secretory phase: increasing Eany increasewhen progesterone primarily (estrogen also stops bleeding Menstrual phase: Withdrawal of Estrogenstimulates totheuterinepresent) endometrium secretes changes luteal hormonal support from wallproliferation oocytesubstances (glycogen, glycoproteins, and endometrium  degeneration of Yitation to79 Yostation's 9feelin mucopolysaccharides) that would support endometrium  menstruation implantation of a fertilized egg/blastocyst 31 Fig. 17.27  Summary: Uterine Changes During the Menstrual Cycle Menstrual Phase- day 1 to day 3-5 – Uterine smooth muscle undergoes rhythmic contractions mediated by prostaglandins produced locally by the endometrial cells causeofcramping higher – Arterioles ofprostaglandins levels severe cause dilate causingcramping astronger rupture contractions of capillaries  blood and endometrial debris make up menstrual flow – Thin layer remains to regenerate the endometrium for the current cycle Proliferative Phase- day 3-5 until ovulation (~day 14) – As estrogen levels increase, endometrium regenerates and thickens – Myometrium (smooth muscle layer) also grows – Progesterone receptors are synthesized/expressed on endometrial cells Secretory Phase- Ovulation to beginning of menstrual flow – Progesterone mediates the secretory phase – Endometrial glands fill with glycogen – Increased # blood vessels and blood flow – Increase of enzymes needed if fertilization occurs – Inhibition of prostaglandins and smooth muscle contractions by progesterone – If fertilization does not occur, around day 25, progesterone and estrogen from corpus luteum begin to decrease causing… …Constriction of blood vessels leads to decreased blood flow so less O2/nutrients delivered which leads to death of endometrial cells …Epithelial lining of uterus (endothelium) degenerates…by day 28, return to Menstrual phase…next cycle begins 32 Figure 17-18 Summary: Hormone Fluctuations During Menstrual Cycle Although GnRH is not shown here, changing pulses of GnRH control other hormonal changes. In early follicular phase: rise in FSH and LH stimulates follicle development past early antral stage (proliferation of granulosa and theca). Estrogen begins to increase by mid-follicular phase- inhibits FSH (indirectly) and LH (directly and indirectly) In late follicular phase, high estrogen stimulates FSH (indirectly) and LH (directly and indirectly) In the luteal phase, high progesterone and estrogen together inhibit LH and FSH secretion (by decreasing GnRH pulse frequency + 33 direct effect on LH from ant. pit.) Summary of Uterine changes during the menstrual cycle Fig 17.27 2o oocyte 34 Fig. 17.27 Figure 17-17: Summary After puberty, maturation of follicles past early antral stage, and release of a 2o oocyte is cyclical, not continuous, in females. Uterine Events: Menstrual then Proliferative Secretory (10-25 Follicles) Stimulated by LH Surge 35 (All others undergo atresia)  Maturation from primordial follicle early antral follicle does NOT require FSH and LH and so can occur between birth and puberty and during menstrual cycles. Atresia occurs here if FSH and LH levels do not increase to continue Summary of follicle development maturation. Theca Granulosa 2-4 million at birth- house 1o oocytes ~400 1st meiotic division dominant and follicles develop after puberty (1/cycle) 2o oocyte to Fallopian tube Maturation from early antral follicle dominant follicle ovulation occurs after puberty only, under the influence of FSH and LH, etc. Non-dominant follicles undergo atresia. 36 What you should have learned: Menstrual cycle – Uterine changes: Menstrual phase, Proliferative phase, Secretory phase How do the phases align with the ovarian phases? What hormonal changes are involved in each uterine phase? 37  2-2 B New material on menopause and hormone replacement therapy- HRT), Questions to help you apply information. 38  Natural Menopause Menopause Cessation of menstruation due to loss of functioning ovarian follicles Process is considered to be complete when it has been 12 months since the last menstrual period Average age of menopause= 51-52 years (typical range 48-55 yrs) Much confusing terminology related to menopause (not tested) Menopausal transition: variability of bleeding is increased and symptoms occur Perimenopause: time immediately prior to menopause and including the first year after menopause Climacteric: includes perimenopause, but extends for longer before and after Premature menopause occurs before age 40 Induced menopause- occurs due to surgery or treatment that removes or destroys ovarian function ex chemotherapy Signs of climacteric: Missed and/or unpredictable menstrual periods Hot flashes - irregular onset of vasodilation of skin arterioles - last 3-5 minutes but may last 60 minutes - Occurs for 6 months to 2 years from onset of climacteric - 75% of females over 50 have hot flashes Periods of emotional irritability _____________________________________________________________ Oldest verified birth - via in vitro fertilization with donor eggs 39 Sept, 2019- 74 year old in India gave birth to twins  2016 and 2022 Menopause articles 1. Menopause Management — Getting Clinical Care Back on Track – JoAnn E. Manson, M.D., Dr.P.H., and Andrew M. Kaunitz, M.D. – n engl j med 374;9 nejm.org March 3, 2016 The New England Journal of Medicine Downloaded from nejm.org at UNIVERSITY OF MICHIGAN on February 4, 2023. 2. The 2022 hormone therapy position statement of The North American Menopause Society (NAMS) – Menopause: The Journal of The North American Menopause Society. Vol. 29, No. 7, pp. 767-794 – DOI: 10.1097/GME.0000000000002028 – © 2022 by The North American Menopause Society Accessed February 4, 2023 Terminology HRT = hormone replacement therapy, now called HT = hormone therapy 40  Major points of 2016 perspectives article 75% of females report perimenopausal symptoms (e.g., hot flashes, night sweats) for 10 years or more – Significant quality of life issues occur such as: lack of sleep, mood changes, issues with concentrating, impaired short-term memory – Untreated symptoms also increase health care costs and cause decreased work productivity – There are effective and safe systemic hormonal (currently most- effective) and non-hormonal treatments (see next slide) 45% of females report vulvovaginal atrophy (genitourinary syndrome of menopause) – Impairs physical health, sexual health, and quality of life – Can be treated effectively and safely with low-dose vaginal estrogen Doctors are not appropriately trained to manage menopausal symptoms – Many females therefore do not get appropriate treatment 41  Summary of newSystemic HTHT:data CEE = conjugated equine estrogens (those w/o uterus) CEE+MPA = conjugated equine estrogens + medroxyprogesterone acetate (those w/uterus) Females were 50-59 years of age Value is events in HT group minus events in placebo group Events = events/1000 females over 5 years Example: 2.5/1000 = slight risk (0.25%) with HT; -2.5/1000 = slight benefit (0.25%) with HT Table found in citation 1 on previous slide; created from data in the following article: Menopausal Hormone Therapy and Health Outcomes During the Intervention and Extended Poststopping Phases of the Women's Health Initiative Randomized Trials – Manson, JoAnn E, MD, DrPH; Chlebowski, Rowan T, MD, PhD; Stefanick, Marcia L, PhD; Aragaki, Aaron K, MS; Rossouw, Jacques E, MD; et al. JAMA: The Journal of the American Medical Association; Chicago Vol. 310, Iss. 13, (Oct 2, 2013): 1353-68. 42  NAMS 2022 Position statement (I won’t test you on the details of this) (citation 2 on slide 5); copied exactly Hormone therapy remains the most effective treatment for vasomotor symptoms (VMS) and the genitourinary syndrome of menopause and has been shown to prevent bone loss and fracture. The risks of hormone therapy differ depending on type, dose, duration of use, route of administration, timing of initiation, and whether a progestogen is used. Treatment should be individualized using the best available evidence to maximize benefits and minimize risks, with periodic reevaluation of the benefits and risks of continuing therapy. For women aged younger than 60 years or who are within 10 years of menopause onset and have no contraindications, the benefit-risk ratio is favorable for treatment of bothersome VMS and prevention of bone loss. For women who initiate hormone therapy more than 10 years from menopause onset or who are aged older than 60 years, the benefit-risk ratio appears less favorable because of the greater absolute risks of coronary heart disease, stroke, venous thromboembolism, and dementia. Longer durations of therapy should be for documented indications such as persistent VMS, with shared decision-making and periodic reevaluation. For bothersome genitourinary syndrome of menopause symptoms not relieved with over-the-counter therapies in women without indications for use of systemic hormone therapy, low-dose vaginal estrogen therapy or other therapies (eg, vaginal dehydroepiandrosterone or oral ospemifene) are recommended. 43 Not on the exam National Cancer Institute at the National Institutes of Health Fact Sheet on Menopausal Hormone Therapy and Cancer is found at the following URL http://www.cancer.gov/cancertopics/fact sheet/Risk/menopausal-hormones 44 Just the Review and Question Slides Please think about and try to answer these before watching the supplement video(s) 45 Review Basics of Follicles 1. Where are the follicles located? 2. What is their role? 3. What part of follicle maturation requires no hormones? 4. What part of follicle maturation requires LH and FSH? 46  Begin with an oogonium prior to 7th month of gestation… Go through the steps AND timing involved in generating an ovum 47 Figure 17.22 Why are estrogen and progesterone low at day 1? Why do FSH and LH begin to rise at day 1? Why does LH plateau and FSH begin to decrease around day 5- 7? 48 Figure 17.22 Why are estrogen levels increasing through mid- late follicular phase? Why does LH suddenly begin to increase significantly? (LH surge) What happens to follicle and oocyte when LH surge occurs? 49 Figure 17.22 What are the roles of estrogen, progesterone, and LH during the luteal phase? 50 Uterine changes are caused by cyclical changes in ovarian hormones. Fig 17.27 (1) What is (2) What is estrogen’s role ovulated? (4) What once it starts changes here that causes increasing secretory around day phase to end? 5ish? (3) What, in general does “secretory” mean? Which hormone is critical for secretory phase? 51 Fig. 17.27 What hormone should I measure to determine if ovulation has occurred? 52  When is a female “fertile”? When could sperm be introduced and possibly lead to fertilization? Range of cycle length is 19-40 days. Think about the timing- which days during each (short, typical, long) cycle could sperm be introduced and result in fertilization? How predictable is it? Is every cycle the same length (see first bullet point)? So, how easy is it to predict when to avoid intercourse to avoid fertilization?...what days should be avoided? 53 Birth Control Pills and other hormone-based contraceptives contain progesterone or progesterone + estrogen. How do they work? 54  What is in “Emergency Birth Control”? Also called “Plan B” 55  The Menopause: what happens to hormone levels? Estrogen level? FSH level? LH level? 56 What you should have learned: Menstrual cycle (Lecture 2) – Uterine changes: Menstrual phase, Proliferative phase, Secretory phase How do the phases align with the ovarian phases? What hormone is measured to determine if ovulation has occurred? Explain how to determine the fertile time during each cycle Mechanism of Hormonal Contraceptive Action Menopause Apply information to solve problems 57