Female Reproductive System PDF

female reproductive physiology MILAGROS B. RABE, MD, MS, PH.D. PROFESSOR IV, DEPT OF PHYSIOLOGY UERMMMCI COLLEGE OF MEDICINE [email protected] OBJECTIVES  I. Female reproduction system  A. Discuss the functional anatomy of the female reproductive tract   A. Give the function of the different or...

female reproductive physiology MILAGROS B. RABE, MD, MS, PH.D. PROFESSOR IV, DEPT OF PHYSIOLOGY UERMMMCI COLLEGE OF MEDICINE [email protected] OBJECTIVES  I. Female reproduction system  A. Discuss the functional anatomy of the female reproductive tract   A. Give the function of the different organs in the female reproductive tract  Discuss the reproductive function of the ovaries: follicular development and gametogenesis  Discuss the endocrine functions of the ovaries. B. Discuss the menstrual cycle 1. Give the phases – ovarian phases, uterine phases 2. Discuss the phases of the endometrial and ovarian cycles. 3. Correlate the changes in blood levels of FSH, LH, estradiol, progesterone and inhibin with the structural changes In the endometrium and ovary during the menstrual cycle. 4. Describe the process of ovulation. C.. Discuss the regulation of the menstrual cycle 1. Give the functions and regulation of LH and FSH. 2. Review the Hypothalamo-Pituitary-Target gland axis.  II. Discuss the changes in pregnancy  II.A. fertilization  II.B. Pregnancy  Describe the anatomic changes  Describe the hormonal changes  Give the basis of the pregnancy test  Give the hormonal parameters of uterine health in pregnancy A. functional anatomy of the female 3 reproductive tract Internal reproductive organs in the female 1. organs (a)principal organs: the ovaries, uterine tubes, uterus, and vagina. (b)the ovary and the relationship of its main supporting mesenteries, the mesovarium, and the mesosalpinx of the broad ligament. (c)A sectioned ovary, indicating the medulla and cortex, with follicles of several different sizes in the cortex Ovarian follicles   Follicle- functional unit of the ovary functions : 1. the development of follicles (folliculogenesis) to produce the mature ovum (oogenesis) 2. Formation of ovarian hormones (endocrine function) 2. Reproductive function of the ovary: folliculogenesis  all of the 7M primordial follicles are formed during the fetal life, formed by mitosis  Follicular atresia (A) at 6 and 9 months' gestation, a marked loss of oocytes due to apoptosis  at puberty only 300,000 remain and continue to decline progressively due to recruitment for each menstrual cycle, until very few and none remain after the menopause at ~50 years of age A B C https://www.ncbi.nlm.nih.gov/books/NB K278951/?report=reader 3. reproductive function of the ovaries  oogenesis = gametogenesis in females  oogonia =ovarian stem cells formed during  fetal development, and divide via mitosis oogonia form primary oocytes (2n) in the fetal ovary prior to birth are then arrested in prophase I stage of meiosis I (diplotene stage), only to resume it at puberty and continues until near menopause (when it ends)  LH surge  ovulation resumption of meiosis in the primary oocyte to form a secondary oocyte (n) , arrested at metaphase II  it completes meiosis only after sperm fertilizes the egg. The release of the polar body also occurs.  In oogenesis, only 1 out of 4 daughter cells survive (secondary oocyte) because the 3 polar bodies die  * meiotic arrest - due to lack of meiosis associated proteins in the developing oocyte https://opentextbc.ca/anatomyandphysiology/chapter/27-2anatomy-and-physiology-of-the-female-reproductive-system/ development of mature Graafian follicle   a.phase 1- preantral or gonadotropin-independent phase  characterized by the growth and differentiation of the oocyte;  This phase is regulated mainly by locally produced growth factors (from the ovary itself)  cuboidal granulosa cells appear proliferate and become multi layered epithelium (secondary follicle) 3 -6 layers paracrine factors stromal cells to become epithelioid thecal cells (flat cells around the follicle) mature pre-antral follicle= oocyte secretes proteins to form the zona pellucida activation growth growth Follicles develop through primordial, primary, and secondary stages before acquiring an antral cavity. 1 2 b. Phase 2 –antral or gonadotropin-dependent phase  is characterized by the tremendous increase of the size of the follicle itself (up to approximately 25-30 mm); 25 days;    increase # granulosa cells  2 groups:  1) stratum granulosum= forms outer wall of follicle  2) cumulus cells= inner cells around the oocyte regulated mainly by FSH and LH (gonadotropins from the anterior pituitary) and also by local growth factors. during the antral stage--- most follicles undergo atresia; however, under optimal gonadotropin stimulation that occurs after puberty, a few of them are rescued (Cyclic recruitment) to reach the pre-ovulatory stage– dominant follicle selected has most # FSH receptors Development of pre-antral to antral follicles  Pre-antral follicles – in development, display an increase in the number of FSH receptors (FSHR)  Effects FSH on the granulosa cells: 1. 2. 3.  granulosa cell proliferation, ~ antrum formation, ~ activation of aromatase enzyme and synthesis of estradiol main factor for selection of pre-antral follicles to convert them to antral stage is their number of FSH receptors that allows it to respond to FSH. (dominant follicle) Williams, CJ & Gregory F Erickson GF. (Jan 30, 2012). Morphology and Physiology of the Ovary. In Endotext. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK278951 Summary: folliculogenesis  process of folliculogenesis occurs within the cortex of the ovary ↳  four major developmental events in folliculogenesis   1) primordial follicle recruitment or primordial follicle activation. ~ 2) pre-antral follicle development; ~  3) selection and growth of the antral follicle; and v  4) follicle atresia - death of the pre antral follicles not selected~ The cortex consists of the surface epithelium (se), tunica albuginea (ta), ovarian follicles (primordial, primary (pf), secondary (sf), small, medium, large Graafian follicle (gf)) and corpora lutea (cl). https://www.ncbi.nlm.nih.gov/books/NBK278951/?report=reader Local hormones produced by the developing follicle During folliculogenesis:  During folliculogenesis, the granulosa cells secrete hormones that produce effects: > development - 1. Inhibin A - produced by granulosa cells from the selected dominant antral follicle after ovulation, inhibit = development of the other primordial follicles after selection of antral follicle at ovulation - -growth 2. inhibin B- produced by mural granulosa cells in the follicular phase that negatively feeds back on FSH secretion prior to ovulation  stop growth of other non-selected follicles Williams, CJ & Gregory F Erickson GF. (Jan 30, 2012). Morphology and Physiology of the Ovary. In Endotext. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK278951 4. Endocrine function of the ovary: 2 cell, 2 gonadotropin theory ovarian steroids are synthesized from cholesterol through the cooperative interactions of theca and granulosa cells. Ovarian steroids teca-> -granulosa :  cells Theca cells : have LH receptors that bind to luteinizing hormone (LH) from the anterior pituitary and stimulates the expression of the enzymes necessary for androgen production (androstenedione) from cholesterol > Theca > (I receptors > androstendione - - -  Androstenedione produced by theca cells diffuse into granulosa cells W  Granulosa cells : have folliclestimulating hormone (FSH) receptors and bind FSH from the anterior pituitary to and synthesize enzymes necessary for estrogen synthesis (estradiol) G -) granulosa cells - > FSH receptors > estrogen Synthesis - - ↓ testosterone extradio B. Menstrual cycle  is the cyclic, orderly sloughing of the uterine lining, in response to the interactions of hormones produced by the hypothalamus, pituitary, and ovaries. 1st day of menstrual bleeding to the onset of menses in next cycle.  phases of menstruation:   (1) follicular or proliferative phase, and  (2) the luteal or secretory phase. cycle length 25 to 30 days with median duration of 28 days  polymenorrhea= menstrual cycles that occur at intervals less than 21 days  oligomenorrhea= menstrual cycles greater than 35 days, are termed  30 ml typical volume of blood lost during menstruation 1. Phases: ovarian cycle B.1.1 Follicular phase begins from the first day of menses until ovulation  Folliculogenesis begins during the last few days of the preceding menstrual cycle until the release of the mature follicle at ovulation.  Increase in FSH receptor numbers is due to an increase in the population of granulosa cells, the one with most FSH receptors– selected as dominant follicle  Increasing # of granulosa cells serum estradiol levels rise in parallel to the growth of follicle  FSH is elevated in early follicular phase, then declines until ovulation;  estrogen causes regeneration of endometrium; of the uterus, the glands are straight and parallel, with little secretion  inhibin B is predominantly secreted by granulosa  cells of pre-antral and small antral follicles so its concentration increases & causes FSH decline- this assures single dominant follicle selection * LH is low in early follicular phase * Hall, JE. Chapter 7- Neuroendocrine control of the menstrual cycle. In. Yen & Jaffe’s Reproductive Endocrinology 8th Ed. Physiology, Pathophysiology and Clinical Management. 2019 pages 149-166e5. Available online 22 February 2018. European Journal of Endocrinology (2005) 152 395– 401  Ovulation occurs due to combined action of:   Hypothalamus, pituitary & ovary positive feedback of estradiol on GnRH, followed by gonadotropin release (LH & FSH) causes the LH surge & FSH surge   Occurs day 14 in a 28 day cycle Ovulation occurs approximately 10-12 hours after the LH peak  With the release of the ovum (secondary occyte stage, n) at ovulation, the follicle becomes the corpus luteum -  LH surge stimulates luteinization of the granulosa cells and stimulates the synthesis of progesterone a - temperature rise of approximately 0.7-0.9 degrees F at midcycle because of the effect of progesterone - B.1.2. Ovulation Ovulation  Mechanism of ovulation: - LH & progesterone cause an increase in prostaglandins and proteolytic enzymes, such as collagenase and plasmin #  Activated enzymes digest collagen in the follicular wall, leading to an explosive release of the oocyte-cumulus complex   EFFECTS of ovulation:  Release of the oocyte  stimulates resumption of meiosis and the completion of reduction division in the oocyte  the release of the first polar body B.1.3. LUTEAL PHASE  usually14 days long in most women  remaining granulosa cells becomes = the corpus luteum & predominantly secretes progesterone, Er  prepares endometrium for implantation of the fertilized ovum  Estrogen levels rise again during the mid-luteal phase in parallel with increase in progesterone then decreases at the end of the menstrual cycle  Inhibin A is the predominant form produced during the late follicular and luteal phases of the normal menstrual cycle,  Corpus luteum function begins to decline 9-11 days after ovulation if the ovum is NOT fertilized. - Luteal phase: endometrial changes  endometrial glands become more tortuous and dilated  pseudostratification and vacuolation almost completely disappear and intraluminal secretions become present > endometrial strom becomes edematous -  Stroma 3 E  Stroma mitoses day 21 or 22,= endometrial stroma becomes edematous. > - > precididual  of stromal cells/stromal mitoses day 23, stromal cells surrounding the spiral arterioles appears begin to enlarge and stromal mitoses become apparent. -  enlargement appearance of predecidual cells day 24, predecidual cells appear around the spiral arterioles and stromal mitoses become more apparent. under - > predecidua differentiates surface day 25, the predecidua begins to differentiate under epithelium the surface epithelium.  day 27, there is a marked lymphocytic infiltration and the upper endometrial stroma appears as a solid sheet of well-developed decidua-like cells.  day 28,= menstruation begins- if no fertilized ovum is implanted B.1.4. MENSTRUATION   due to declining corpus luteum function- decline in progesterone levels  results in increased coiling and constriction of the spiral arterioles  tissue ischemia due to decreased blood flow to the functional endometrial layers, The release of prostaglandins may be due to decreased stability of lysosomal membranes in the endometrial cells  prostaglandins cause contractions of the uterine smooth muscle and sloughing of the degraded endometrial tissue. MENSTRUATION  Menstrual fluid = composed of desquamated endometrial tissue, red blood cells, inflammatory exudates, and proteolytic enzymes;  Average duration of menstrual flow = four to six days  two days after the start of menstruation and while endometrial shedding is still occurring : estrogen produced by the growing follicles :  a. starts to stimulate the regeneration of the surface endometrial epithelium and also  b. causes prolonged vasoconstriction enabling the formation of a clot over the denuded endometrial vessels. B.2. Cervix: changes in quality of mucus secretion 1. after menstruation mucous is scant and viscous; 2. late follicular phase, under the influence of rising estradiol levels, the cervical mucous becomes clear, copious and elastic.  The quantity of cervical mucous increases 30 x compared to the early follicular phase The elasticity of the cervical mucous can be evaluated between two glass slides and recorded as the spinnbarkeit.  under the microscope, the cervical mucous will display a characteristic ferning or palm-leaf arborization appearance. 3. After ovulation, as progesterone levels rise, the cervical mucous once again becomes thick, viscous and opaque and the quantity produced by the endocervical cells decreases. C.1. Review of female reproductive physiology regulation  hypothalamus secretes GnRH, which reaches the gonadotrophs in the anterior pituitary via the long portal veins  GnRH causes synthesize and release two gonadotropins—FSH and LH at the anterior pituitary  LH binds to receptors on theca cells to increase the biosynthesis of progestins and androgens.  The androgens (androstenedione) enter granulosa cells, which convert the androgens to estrogens.  FSH binds to receptors on. granulosa cells to increase the production of steroidogenic enzymes as well as activins and inhibins  The activins and inhibins act only on the anterior pituitary.  The estrogens and progestins act on both the anterior pituitary and the hypothalamic neurons, exerting both positive- and negative-feedback controls. GnRH pulses the pattern of GnRH secretion is essential for the regulation of the menstrual cycle. LH pulse frequency is slow in the luteal phase, and increasingly speeds up during the follicular and the pre-ovulatory phases, presumably reflecting changes in GnRH pulse frequency Ehlers, K, Halvorson, L, Glob. libr. women's med., (ISSN: 1756-2228) 2013; DOI 10.3843/GLOWM.10285 Functions of gonadotropins: Follicle stimulating hormone FSH Luteinizing hormone LH 1. Follicular development 1. Causes the ovulation in the mature Graafian follicle (with the most number of LH receptors) 2. Development of corpus luteum - luteinization of the remaining granulosa cells after the ovulation has occurred 3. Progesterone synthesis by the corpus luteum - Granulosa cell proliferation & differentiation - Antral follicle development 2. Hormone synthesis: - Estrogen - Inhibin B 3. Induction of LH receptors on the dominant follicle C.2. Other hormones: Inhibin, activin & follistatin inhibin - suppresses FSH secretion Activin A- stimulates the release of FSH from the anterior pituitary Follistatin - Binds activin THUS neutralizing the FSH stimulatory actions of activin (de Kretser DM et al. Inibins, activins and follistatin in reproduction. Human Reproduction Update , 2002, 8(6) 529-541 Hiroyuki Kaneko, Follistatin. in Handbook of Hormones, 2016) Wijayarathna R & de Kretser DM. Human Reproduction Update, Vol.22, No.3 pp. 342–357, 2016 Hormones that influence FSH secretion Inhibin  Glycoporteins; glycosylation is essential for bioactivity = (FSH suppressing activity).  produced in gonads only  negative regulation of FSH secretion, directed exclusively at the pituitary and independent of GnRH inputs; (classic endocrine)  paracrine/autocrine actions in gonads by antagonism of activin Activin  homo- dimeric proteins produced in a wide range of tissues  activins stimulate FSH secretion through paracrine mechanisms in the pituitary Follistatin  a single-chain glycoprotein hormone  Binds activin THUS neutralizing the FSH stimulatory actions of activin  no stage-specific changes in the levels of follistatin during the menstrual cycle (Evanset al., 1998; McConnellet al.,1998),  Paracine effect in pitutitary c.3. polycystic ovary 1. irregular periods – which means your ovaries do not regularly ovulate= anovulatory 2. excess androgen – high levels of "male" hormones in your bodymay cause physical signs such as excess facial or body hair, acne Lab tests: Some biochemical signs of androgen excess include: Elevated serum testosterone (total testosterone) Elevated level of free testosterone Elevated dehydroepiandrosterone sulfate, also called DHEA sulphate, or DHEAS 3. polycystic ovaries – your ovaries become enlarged and contain many fluid-filled sacs (follicles) that surround the eggs (but despite the name, you do not actually have cysts if you have PCOS) Often women with PCOS also have insulin resistance– thus also develop diabetes type II McCartney CR, Marshall JC. CLINICAL PRACTICE. Polycystic Ovary Syndrome. N Engl J Med. 2016 Jul 7;375(1):54-64. doi: 10.1056/NEJMcp1514916. PMID: 27406348; PMCID: PMC5301909. II. Pregnancy A. Fertilization : Fertilization = the fusion of male and female gametes that facilitates the development of a new organism  semen comprising millions of sperms are inseminated into the female vagina during coitus. These swim towards the uterus and but only a few reach the opening of the fallopian tube  The secondary oocyte is released from the mature Graafian follicle of the ovary at ovulation and enters into the fallopian tube,   fertilization takes place at the ampulla of the fallopian tube through the fusion of both a single sperm and the secondary oocyte, which results in the formation of a zygote that develops into a new individual. Fertilization :Stages 1. Preparation: Capacitation and acrosome reaction. Acrosomal vesicle fusion is the membrane fusion event of this stage. 2. Binding: Species-specific interaction of gametes and membrane Fusion or Merging of sperm and egg plasma membranes is the membrane fusion event of this stage. 3. Cortical reaction (fusion of cortical vesicles with the plasma membrane of oocyte) releasing enzymes to make the zona pellucida hard and impenetrable by other sperms. This prevents polyspermy– or fertilization by more than 1 sperm. 4. Karyogamy or pronuclear fusion= fusion or merging of 2 nuclei to re-establish the normal chromosomal number of 23 pairs of chromosomes in a human. B. Implantation  Implantation is the process by which the embryo attaches to the endometrial surface of the uterus and invades the epithelium and then the maternal circulation to form the placenta.  window of endometrial receptivity is from days 16-22 of a 28-day normal menstrual cycle, or 5-10 days after the luteinizing hormone (LH) surge  Estrogen and progesterone that increases during the luteal phase prepares the implantation site, at the dorsal wall of the uterus Kim SM, Kim JS. A Review of Mechanisms of Implantation. Dev Reprod. 2017 Dec;21(4):351-359. doi: 10.12717/DR.2017.21.4.351. Epub 2017 Dec 31. PMID: 29359200; PMCID: PMC5769129. II. C. Changes in pregnancy: Blood 1. Plasma volume increases progressively throughout normal pregnancy.   50% increase occurs by 34 weeks’ gestation and is proportional to the birthweight of the baby. expansion in plasma volume is greater than the increase in red blood cell mass so there is a fall in haemoglobin concentration, hematocrit and red blood cell count= haemodilution,  usually no change in mean corpuscular volume (MCV) or mean corpuscular haemoglobin concentration (MCHC). 2. The platelet count tends to fall progressively during normal pregnancy, but remains within normal limits, without an underlying pathology.  So, a pregnant woman is not considered to be thrombocytopenic in pregnancy until the platelet count is less than 100 × 109 cells/l (unless there is an underlying disease) 3. Pregnancy causes a two- to three-fold increase in the requirement for iron, not only for haemoglobin synthesis but also for for the foetus and the production of certain enzymes.  There is a 10- to 20-fold increase in folate requirements and a two-fold increase in the requirement for vitamin B12. II. A. Changes in pregnancy: Blood  4. during pregnancy there is a physiological hypercoagulable state (important for hemostasis following delivery)  concentrations of certain clotting increased.    factors, particularly VIII, IX and X, are Fibrinogen levels rise significantly by up to 50% and fibrinolytic activity is decreased. Concentrations of endogenous protein S decrease. anticoagulants such as antithrombin and Thus pregnancy alters the balance within the coagulation system in favour of clotting, predisposing the pregnant and postpartum woman to venous thrombosis.  This increased risk is present from the first trimester and for at least 12 weeks following delivery  BUT the vitro tests of coagulation [activated partial thromboplastin time (APTT), prothrombin time (PT) and thrombin time (TT)] remain normal in the absence of anticoagulants or a coagulopathy. II. Changes in pregnancy: CVS 1. Venous stasis in the lower limbs is associated with venodilation and decreased flow, which is more marked on the left. This is due to compression of the left iliac vein by the left iliac artery and the ovarian artery. On the right, the iliac artery does not cross the vein. 2. 20% increase in cardiac output by 8 weeks gestation. This is due to peripheral vasodilatation, mediated by endothelium-dependent factors, including nitric oxide synthesis, upregulated by estradiol and possibly vasodilatory prostaglandins (PGI2). Cardiac changes in pregnancy 3. Peripheral vasodilation leads to a 25–30% fall in systemic vascular resistance, and to compensate for this, cardiac output increases by around 40% during pregnancy. This is achieved predominantly via an increase in stroke volume, but also to a lesser extent, an increase in heart rate. An increase in stroke volume is possible due to the early increase in ventricular wall muscle mass and end-diastolic volume (but not end-diastolic pressure) seen in pregnancy. 4. Blood pressure decreases in the first and second trimesters but increases to nonpregnant levels in the third trimester Cardiac changes in pregnancy  There is a profound effect of maternal position towards term upon the hemodynamic profile of both the mother and fetus.  In the supine position, pressure of the gravid uterus on the inferior vena cava (IVC) causes a reduction in venous return to the heart and a consequent fall in stroke volume and cardiac output.  Turning from the lateral to the supine position may result in a reduction in cardiac output.  Pregnant women should therefore be nursed in the left or right lateral position wherever possible (rather than in the supine position)  If the woman has to be kept on her back, the pelvis should be rotated so that the uterus drops to the side and off the IVC, so that the cardiac output and uteroplacental blood flow are optimized.  Why should we avoid this? The Reduced cardiac output is associated with a reduction in uterine blood flow and therefore in placental perfusion, which could compromise the fetus. Cardiac changes in pregnancy  Although both blood volume and stroke volume increase in pregnancy, pulmonary capillary wedge pressure and central venous pressure do not increase significantly.  Pulmonary vascular resistance (PVR) & systemic vascular resistance (SVR), decreases significantly in normal pregnancy.  The colloid osmotic pressure/pulmonary capillary wedge pressure gradient is reduced by about 30%, making pregnant women particularly susceptible to pulmonary edema.   Pulmonary edema will be precipitated if there is either an increase in cardiac pre-load (such as infusion of fluids) or increased pulmonary capillary permeability (such as in preeclampsia) or both. Labor is associated with further increases in cardiac output (15% in the first stage and 50% in the second stage)  Uterine contractions lead to an auto-transfusion of 300–500 ml of blood back into the circulation and the sympathetic response to pain and anxiety further elevate the heart rate and blood pressure.  Cardiac output is increased between contractions but more so during contractions. Renal changes in pregnancy:  Due to renal vasodilatation, the renal plasma flow and glomerular filtration rate (GFR) both increase, compared to non-pregnant levels  the increase in plasma volume causes decreased oncotic pressure in the glomeruli, with a subsequent rise in GFR.  Vascular resistance decreases in both the renal afferent and efferent arterioles and therefore, despite the massive increase in renal plasma flow, glomerular hydrostatic pressure remains stable, avoiding the development of glomerular hypertension.  As the GFR rises, both serum creatinine and urea concentrations are expected to decrease due to increased excretion rate of the metabolites. Endocrine changes in pregnancy  The pituitary gland enlarges in pregnancy mainly due to proliferation of prolactinproducing cells in the anterior lobe.  Serum prolactin levels increase in the first trimester and are 10 times higher at term.  Levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are undetectable during pregnancy due to the negative feedback from elevated levels of estrogen, progesterone and inhibin.  Pituitary growth hormone production is decreased but serum growth hormone levels are increased due to growth hormone production from the placenta.  Oxytocin levels increase in pregnancy and peak at term but the levels of ADH are unchanged. Respiratory changes in pregnancy   There is a significant increase in oxygen demand during normal pregnancy due to a 15% increase in the metabolic rate and a 20% increased consumption of oxygen. There is a 40–50% increase in minute ventilation, mostly due to an increase in tidal volume, rather than in the respiratory rate. B. Hormones in pregnancy Progesterone  largely produced by the corpus luteum until about 10 weeks of gestation. After this period, progesterone is produced by the placenta.  Maintains pregnancy and prevents maternal immunologic response to fetal antigens,  Prepares and maintains the endometrium to allow implantation and maintain endometrial function in pregnancy  Estrogen Produced by the placenta using fetal adrenal androgens http://www.ijem.in on Wednesday, September 28, 2016, IP: 88.75.254.119] B. Hormones in pregnancy Protein hormones:  Human placental lactogen - causes production of insulin like growth factor in the pregnant woman and causes a diabetogenic effect. Indicates health of the placenta  Human chorionic gonadotropin (hCG)  produced primarily by differentiated syncytiotrophoblasts.  stimulates the production of progesterone by the corpus luteum from time of fertilization to the 10th week of gestation, and then subsequently by the placenta, until parturition occurs.  http://www.ijem.in on Wednesday, September 28, 2016, IP: 88.75.254.119] Summary: Hormone levels in menstrual cycle & in pregnancy Pregnancy test: Check presence of HCG in the urine, test strip contains anti-HCG antibodies (colored line) becomes visible if there is HCG in the urine sample.