Reproductive Development & Function of the Female Reproductive System PDF

 111 (2) · Testosterone FsH /It -   Sex chromosomes are the X and Y chromosomes  In genetic female: the cortex develops into an ovary and the  Y chromosome is necessary and sufficient for production of...

 111 (2) · Testosterone FsH /It -   Sex chromosomes are the X and Y chromosomes  In genetic female: the cortex develops into an ovary and the  Y chromosome is necessary and sufficient for production of medulla regress testes.  Y chromosome contains, the sex demining region that coded  Embryonic ovary does not secrete hormones for a protein called SRY protein.  SRY bind DNA and act as transcription factor for many genes  Hormonal treatment of mother has NO effect on gonadal necessary for testicular differentiation “including MIS” differentiation in human (BUT has effect on ductal and genital  Spermatogonium cells (diploid cells) are of XY pattern differentiation)  Male sperm either X or Y pattern  Oogonia cells (diploid cells) are of XX pattern In Boys:  Female ovum is X pattern  In fetal period (before birth): testosterone secreted as burst in male  In neonatal period (after birth): another testosterone burst  genital ridge  Primitive gonads The gonads develops a appear with unknown function cortex and medulla  Thereafter: Leydig cells become quiescent  Until 6 weeks of development the gonadal structure is  At puberty: Leydig cells are activated by pituitary gonadotropin identical in both sexes. (LH)  In genetic male: the medulla develops (during 7-8 weeks) into In Girls: a testis and the cortex regress  Thelarche: development of breast  Leydig and Sertoli cells appear and secrete testosterone  Pubarche: development of axillary and pubic hair and MIS  Menarche: first menstrual period  MIS causes regression of mullerian duct by apoptosis  Adrenarche: increase in adrenal androgens (DHEA) at 8-10 in girls and 10-12 in boys “increase in 17α-hydroxylase activity” · · bedr - Removal of gonads: Cortex Cortex 335)mullaa se  If during the period from soon after birth to puberty: Only a small increase in gonadotropin (FSH) secretion des ,  If during adulthood: a high increase in FSH secretion Leptin:  Leptin, the satiety-producing hormone secreted by fat cells, may be the link between body weight and puberty.  Obese ob/ob mice that cannot make leptin are infertile, and their fertility is restored by injections of leptin.  Leptin treatment also induces precocious puberty in immature female mice. Causes of hot flashes:  Young women who engage in strenuous athletics lose weight will stop  They occurs when ovaries loose their function menstruating. If these girls start to eat and gain weight, they (occurs when early menopaused is produced by menstruate again, that is, they “go back through puberty.” bilateral ovarioctomy) menopause : Definition: Unresponsiveness of ovaries to gonadotropins with  They coincide with surges of LH secretion that disappearance of sexual cycle with advancing age secreted in episodic bursts at interval of 30- Cause: decline in the number of primordial follicles at time of menopause 60min or more (Circhoral secretion), and in (i.e.; loss of ovarian function) absence of estrogen and progesterone theses burst are large. Each hot flash begins with the During menopause: start of a burst. 1. The ovaries no longer secrete progesterone and 17β-estradiol in appreciable quantities.  LH itself is not responsible for hot flashing (they 2.Estrogen is formed only in small amounts by androstenedione appear after removal of pituitary) aromatization in peripheral tissues 3.The uterus and vagina gradually become atrophic al  Some estrogen-sensitive events in 4.FSH secretion increase and FSH plasma level increase to high levels hypothalamus initiates both the LH bursts and and LH levels moderately high. These due to reduced –ve feedback the episodes of flashing inhibition of estrogen and progesterone on pituitary gland Onset: 45 to 55 years of age (average 52). - & Boy temperature  Rise starts 1-2 days after ovulation  Temp. recording must be in the morning before getting out of bed  The rise is probably due to increase in progesterone secretion (progesterone is thermogenic hormone) Recording ovulation time and fertile period  LH surge (in the midcycle; i.e.; at day 14) trigger ovulation  Ovulation occurs ~ 9hr after the peak LH surge  The ovum lives ~ 72hr after extrusion from the follicle (after ovulation)  BUT the ovum fertilizable for a much shorter time than 72hr.  Fertile period is 48hr (2days) before ovulation. Estrogens Estrogen Functions  Binding to plasma protein: Estradiol 98% [60% to  Ovarian follicle growth albumin and 38% to gonadal steroid-binding globulin  Increase uterine tube (oviduct) motility (GBG) while the free circulating fraction is 2%.  Cyclic change in endometrium (proliferation)  GBG also binds testosterone.  Make the cervix mucus thin and alkaline to promote survival of sperm  Liver Metabolism: estradiol, estrone, and estriol are  Cornified the vaginal epithelium (converted to hard metabolized by glucuronide and sulfate conjugation. tissue “from cuboidal to stratified form”)  Increase uterine blood flow (necessary for secretory  Renal excretion: estradiol, estrone, and estriol and phase) their other metabolites are excreted in the urine.  Promote more active excitation (contraction) of uterine smooth muscles (myometrium), i.e.; increase  Enterohepatic circulation: Appreciable amounts are force and frequency of contraction secreted in the bile and reabsorbed into the  Estrogen increase sensitivity of uterine smooth muscle bloodstream (enterohepatic circulation) to oxytocin.  They inhibit FSH secretion (-ve feedback)  In some circumstances they inhibit LH secretion (–ve feedback) and in other increase LH secretion (+ve feedback)  They inhibit implantation of ovum when given in larger & doses for 4-6days when use as morning-after  Estrogen source: ovary contraceptives  Estradiol secretion rate in men: 50 g/day  Promote breast enlargement at puberty in girls  Produce ductal growth in the breast  Responsible for the pigmentation of areolas at puberty and during pregnancy  Promote breast enlargement at puberty in girls Estrogen receptors  Produce ductal growth in the breast  nuclear receptors  Responsible for the pigmentation of areolas at puberty  Act by gene transcription and during pregnancy  They are ERα and ERβ  ERα presents in Uterus, Kidney, Liver, Heart  ERβ presents in Ovaries, prostate, lung, GIT, Bone  Estrogen produce body changes characteristics of marrow and CNS female 1. Enlarge breast (and uterus and vagina)  Most effects of estrogen are genomic (production of 2. Narrow shoulders mRNA) 3. Broad hips  BUT nongenomic effects are possible to explain the 4. Thighs that converge rapid effect on neuronal discharge and –ve feedback 5. Arms that diverge (wide carrying angle) on FSH 6. Fat distribution in breast and buttocks 7. Voice stay high-pitches because larynx retain its prepubertal proportions (male voice is Bass) 8. Less body hair 9. More scalp hair 10.Flat-topped pubic hair (female escutcheon) Note:  These changes are due in part to estrogen and in part to absence of testicular androgens  Fat distribution in breast and buttocks also seen in castrated males  Growth of pubic and axillary hair in male and female is due primarily to androgens rather than estrogens S