Reproductive System Flashcards
Male/female commonalities
Gamete formation and hypothalamic/pituitary control of reproduction
Gametogenesis
Each has 23 chromosomes and is formed by meiosis
Mitosis vs meiosis
Mitosis: somatic cells and has 1 DNA replication/cell division
Meiosis: Gametes and has 1 DNA replication/2 cell divisions and has a recombination
Meiosis 1 and 2
1) divides # of chromosomes
2) divides sister chromatids (similar to mitosis)
Hypothalamic pituitary control
Regulated by negative feedback
GnRH
Secreted in pulses from neuroendocrine cells in the hypothalamus to release LH or FSH
GnRH pulsatility
Low-frequency GnRH is FSH, high-frequency GnRH is LH. Pulsatility changes during development
Testes
A primary endocrine gland in males that produces sperm
Vas deference
Recieve empty secretions from the seminal vesicles and passes through the prostate
Male urethra
Shared by the urinary and reproductive system
Sertoli cells
Support sperm development by absorbing nutrients and putting waste in the blood
Leydig cells
Interstitial cells that secrete testosterone
Blood-testies barrier
Made of tight-junctions to ensure blood cells and immune cells don’t come in contact with sperm
Spermatogenesis
Occurs in seminiferous tubule near Sertoli cells.
1) A spermatogonium divides via mitosis and stays to produce more and other undergoes meiosis (primary spermatocyte)
2) spermatocyte travels through tight junctions and creates 4 spermatids after meiosis II
3) spermatids mature to spermatozoa
Spermatozoa structure
Nucleus takes up most of the cell, acrosome head contains enzymes to breakdown egg coat, mitochondria at tail for swimming
Sperm pathway
Vas deferens > past seminal vesicles > past prostate > bulbourethral glands > outside
Semen contents (5)
1) 1% spermatozoa
2) Mucous (lubricant)
3) buffers
4) nutrients
5) prostaglandins (smooth muscle contraction)
Semen transfer regulation
PSNS causes penile arterioles to dilate and cause an erection. SNS inhibits this
Inhibin
Secreted by testies and stimulates negative regulation of FSH
FSH and LH
FSH: stimulates Sertoli cells which secretes androgen-binding proteins
LH: stimulates Leydig cells which secretes testosterone
Testosterone synthesis
Cholesterol > progesterone > testosterone
Testosterone as a precursor
Aromatase > estradiol
5 alpha-reductase > DHT
Testosterone functions
Promotes spermatogenesis, maintain reproductive tract, increases sex drive, feedback on GnRH, LH, FSH, etc
5 alpha reductase inhibitors
Can be used to treat benign prostate enlargement and male pattern baldness
Oogenesis (fetal stage)
Primordial germ cells go through mitosis and become oogonia. Oogonia enter meiosis I but cell division doesn’t occur
Oogenesis (puberty)
One primary oocyte completes meiosis I and enters meiosis II to become a secondary oocyte every 28 days.
Oogenesis (ovulation)
Released oocyte from meiosis II receives more cytoplasm than polar body and completes meiosis II if fertilized to become a secondary oocyte
Oogenesis and spermatogenesis
Oogenesis has asymmetric cell division, only one secondary oocyte from each oogonium, limited duration, limited number of primary oocytes
Oocyte maturation
Primary follicles surround oocytes in stasis until puberty, maturation recruits 5-10 follicles (1 matures) and the rest die
Granulosa cells
In follicles and surround the oocyte to support development
Theca cells
Secrete steroid hormone precursors
Menstrual cycle components
Ovarian and uterine cycles. Follow hormonal fluctuations (28 days)
Ovarian cycle summary
First half is the follicular phase (1-14), second half is the luteal phase (15-28)
Uterine cycle summary
Menses phase (1-5), proliferative phase (5-14), secretory phase (14-28)
Menses phase
Blood vessels supplying endometrium constrict and shed the lining. Decreased progesterone and estrogen
Proliferative phase
Endometrium thickens as blood supply is re-established. Estrogen increases
Secretory phase
Glands in the endometrium secrete viscous fluid. Increased progesterone and estrogen
Estrogen release
Follicles make estrogen, so more is increased during the follicular phase and luteal phase
Progesterone release/ function
Low during follicular phase, spikes after ovulation. Increases pituitary sensitivity to GnRH
Early to mid-follicular phase
1) LH stimulates release of androgens from theca cells
2) FSH stimulates estrogen from granulosa cells
3) Granulosa cells secrete AMH to prevent follicle recruitment
4) estrogens exert positive feedback on granulosa and negative on FSH and LH
Late follicular phase
1) tertiary follicle present to secrete inhibin (inhibits FSH), progesterone and estrogen. High estrogen increases GnRH pulse frequency (causes LH to trigger meiosis I completion)
Early to mid-luteal phase
Drop in LH and FSH. Corpus luteum releases progesterone, inhibin and estrogens. Progesterone increase and estrogen inhibit GnRH
Late Luteal phase
Occurs when no fertilization occurs. Drop in progesterone, estrogen and inhibin due to corpus Albicans. GnRH turns on again
Androstenedione synthesis
Made by theca cells and triggered by LH.
Androstenedione as a precursor
Converted to estrone by aromatase and eventually estradiol in granulosa cells
Estrogen functions
Promote follicular development, endometrium growth, negative feedback on GnRH, etc
Adrenal Androgens
Increase sex drive and cause pubic hair growth
Menopause
End of the female reproductive cycle. Ovaries can’t respond to FSH and LH, estradiol and progesterone levels fall, no negative feedback for FSH and LH increase
Fertilization
Sperm guided by chemotaxis (progesterone around oocyte) tunnel through oocyte barriers and fuse with it
Acrosomal reaction
Sperm docks on oocyte and depolarizes it, triggering the completion of meiotic division and fusion of egg and sperm nuclei
Trophoblast
Precursor to the embryo and other structures such as placenta. Secretes hCG
hCG function
Maintains the corpus luteum to prevent the next menstrual cycle. Stimulates fetal testis. Basis of pregnancy tests
Placenta role
Preforms digestive, respiratory and renal system in fetus and exchanges nutrients/waste
Maternal vasculature
Not linked to fetal vasculature, maternal blood forms a lacuna and fetal chorionic villi transfer materials
Progesterone in pregnancy
Suppresses uterine contractions, cervical plug, mammary gland development
Estrogen in pregnancy
Uterine development, breast duct development, etc
Human placental lactogen
High in mother, low in fetus. Decreases maternal glucose uptake and enhances maternal lipolysis
First trimester
0-12 weeks, embryo development
Second trimester
12-28 weeks, fetal development
Third trimester
28 weeks to delivery (37-42 weeks)
Maternal adaptation to pregnancy
Increased vasopressin, increased cardiovascular output, partially suppressed immune system, hyperparathyroidism
Relaxin
Released before labour from the ovary and placenta to loosen ligaments in the pelvis
Labour trigger
Increased estrogen/oxytocin receptors in uterus, increased fetal cortisol, CRH and prostaglandins
Labour mechanism
Positive feedback loop caused by cervical strecth
Prolactin
Stimulates epithelial milk-producing cells after labour. Released from pituitary
Oxytocin and breast milk
Contracts myoepithelial cells to release milk from cells. Released from pituitary
Breast milk inhibition
Estrogen and progesterone inhibit milk production. Prolactin inhibitory hormone from hypothalamus downregulates prolactin
Fetal development at 6 weeks
Bipotential primordial can develop into ovaries or testies based on sex chromosomes
XX development
Mullerian duct becomes female structures. Absence of AMH allows this to occur. Wolffian duct regresses
XY development
Wolffian duct turns into male reproductive structure due to testosterone presence. AMH secreted
SRY
Gene only on Y chromosome that encodes TDF (testes-determining factor) and SOX9. Needed for male phenotype
SOX9
Transcribes SF1 and AMH for Sertoli, Leydig and testes development
Sertoli cells in sex differentiation
Secrete SMH
Leydig cells in sex differentiation
Secrete testosterone for Wolffian development.
DHT synthesis/function
Testosterone turned into DHT by 5-alpha reductase. Forms external male genitalia
B-catenin
Suppresses SOX9 expression for the development of female tissues
Atypical androgen synthesis in XY
Can’t made hormones due to 5-alpha reductase deficiency. No external male genitalia
Androgen insensitivity
Causes testosterone receptors to not function properly. Also results in no testosterone derivatives
What are androgens
Hormones that play a role in male traits and reproductive activity. Present in both sexes
