Reproduction Flashcards
Chimerism
Different zygotes that fuse during development
Mosaicism
Different genotypes in different cells arising from the same zygote
Differentiation of internal genital ducts
Testosterone from leydig cells–> keep wolfian
Anti-mullerian Hormone from sertoli cells–> degrade mullerian (female). (AMH also further develops and stimulates leydig cells)
Wolffian ducts
Become epididymis, vas deferens, seminal vesicles and ejaculatory duct. Preserved via testosterone secretion from leydig cells.
Mullerian ducts
Become fallopian tube, cervix and upper vagina. Regress in presence of AMH. Normal sized growth requires estrogen.
Propecia
Blocks function of 5-a reductase and therefore DHT functioning
Turner’s Syndrome
XO
Streak instead of ovary
Otherwise fully female
Androgen Resistance
Male Pseudohermaphroditism
XY, but body isn’t affected by the testosterone so look female and have female genitalia
Klinefelter’s Syndrome
XXY
Phenotypically male (due to Y chromosome)
Infertile, no spermatogenesis or semniferous tubules. Some gynecomastia, and female pattern pubic hair. Decreased upper/lower segment ratio.
Kallmann’s Syndrome
Anosmia and microphallus
Female Pseudohermaphroditism
XX
Caused by very early androgen exposure. Labia fuse to form penile urethra. Urogenital sinus is retained. Advanced skeletal age so get tall fast then stop growing. Clitoromegaly and other ambiguities.
True hermaphrodites
Both gonadal sexes present, often as an “ovotestis”. Fertility has been reported in some patients. Highly variable external genitalia. Often have cryptorchidism (1 descended testicle) or hypospadias (urethra in wrong location).
LH stimulates what cells in males? What does FSH stimulate?
Leydig to release testosterone (via control of cholesterol –> pregnenolone conversion)
Sertoli to release AMH
ABP
Androgen binding protein.
Produced by the Sertoli cells and binds to T/DHT. Works to keep “T” levels high near the developing sperm
Source of all circulating DHEA
The adrenal cortex
Percent of testosterone which is free
2%
DHT and prostate cancer
Prostate growth and cancer is partly androgen dependent. 5a-reductase inhibitors (Propecia) and androgen receptor blockers (flutamide) can reduce growth. Long term, non-pulsatile GnRH can also shut down LH.
Spermatogenesis
Overall umbrella term for the process of sperm production
Spermiogenesis
Cellular remodeling of spermatids into spermatozoa. Nuclear condensation, tail development, shrinkage of cytoplasm, acrosome development
Spermeation
Extrusion of flagellated spermatozoa into the lumen of the tubule
Spermatogonia
Pool of undifferentiated cells which are outside the blood/testis barrier and later commit to differentiation to spermatozoa
What 2 sperm cell types are connected by intracellular bridges and for what purpose?
Spermatids and secondary spermatocytes. This allows for synchronization of a group of cells and allows sharing of resources.
Sperm meiosis
1st division: primary spermatocytes –> 2ndary
2nd division: 2ndary spermatocytes –> spermatids
Epididymis Function
Reservoir for sperm. Sperm maturation and stabilization of acrosome
Prostate
Alkaline secretions to neutralize vaginal secretions
Seminal Vesicle
Secretions of prostaglandins to contract uterus and fallopian tubes which aids in sperm movement
What directly blocks hypothalamic GnRH release? What activates it?
BLOCKS: Dopamine, Endorphins, T/E2
ACTIVATES: NE
Sertoli cell function
- stimulates ABP biosynthesis (keeps T high near developing cell
- activates aromatase converting T to E2
- increases spermatic growth factors
- increases inhibin (positive paracrine feedback to stimulate T secretion)
- secretes AMH
- contributes to blood/testes barrier
What triggers the spinal reflex of ejaculation?
The entry of semen to the bulbous urethra from the prostatic urethra
Stages of meiosis that the eggs are in
By 6 months after birth, all eggs are primary oocytes, arrested in prophase I.
Just before ovulation, it begins moving through meiosis and will eventually arrest in metaphase II (after ovulation).
What is needed for primary follicles to become secondary?
Influence of FSH
Graafian follicle
Dominant follicle with antrum and surrounding zona pellucida. This one will increase with antral fluid until bursting, becoming the one which ovulates.
What happens to the Graafian follicle subsequent to ovulation?
It’s granulosa and theca cells differentiate to the corpus luteum.
Corpus luteum
- secretes progesterone
- provides gonadal steroids that optimize implantation and maintain zygote until placenta is formed
What happens to the corpus luteum if there is no fertilization?
Luteolysis. It regresses and becomes necrotic, forming a CORPUS ALBICANS.
Inhibin B release vs. Inhibin A
B is mainly from the dominant follicle. A is from the corpus luteum.
Main carrier for Estradiol
SHBG (Sex hormone binding globulin)
Main carrier for progesterone
CBG (corticosteroid binding globulin)
What kind of hormones are activin and inhibins?
Peptide
Follistatin function
Binds activin, reducing its effective concentration.
Clomid
estrogen receptor antagonist that actually ended up causing fertility by blocking LH/FSH negative feedback
The phases of the menstrual cycle
(1) FOLLICULAR: time of follicular growth. Represents variable time.
(2) OVULATORY: final oocyte maturation/release
(3) LUTEAL: corpus luteum formation and release of hormones. Prolonged in pregnancy
Hormones during follicular phase
developing follicle releases E2. E2 + inhibin from ovary feedback to turn-down pituitary.
E2 [ ] reaches certain threshold.
Inhibin B increases production of what cells?
Androgen production by THECA CELLS of ovary.
Ovulatory phase hormones
Once E2 has reached threshold during follicular, it switches to positive feedback.
Continues to feedback until LH surge occurs.
Rupture of follicle causes E2 to decrease.
Follicle begins to form CL.
Luteul phase hormones
CL secretes lots of E2 and progesterone. E2 has strong negative feedback blocking FSH/LH/GnRH. This loss of LH –> degradation of CL w/o HCG rescue.
Key actions that cause formation of secondary follicles
(1) Theca ells proliferate and develop LH receptors
(2) Granulosa cells acquire receptors for FSH, androgens and estrogens.
Actions of E2 from Graafian
(1) inhibit growth of cohort follicles
(2) alter cervical mucus to aid sperm transport
(3) prep fallopian tube for transport
(4) prep endometrium
(5) prime GnRH to evoke LH surge
2 compartment method
Facilitates female conversion of cholesterol to E2.
Granulosa cells: aromatase
Theca cells: androgens (androstenedione) + vascularization for actual release
Cyclic changes in female reproductive tract
PROLIFERATIVE PHASE: dominated by estradiol. late follicular phase. endometrium growing.
SECRETORY PHASE: progesterone dominated. ovulatory phase. carb rich mucus.
ISCHEMIC PHASE: declining progesterone. restriction of spiral arteries + necrosis
Vaginal epithelial cells in follicular vs luteal
FOLLICULAR (lots of estrogen): large, squamous, cornified.
LUTEAL (lots of progesterone): small, basophilic.
Dysmenorrhea
Painful menses related to uterine contractions that may involve pelvic pain radiating to back and thighs, nausea, vomiting, diarrhea.
Large levels of prostaglandins
Virilization
Hirsutism + clitoral hypertrophy, voice deepening, temporal balding, male pattern skeletal development.
Treaments for PCOS
-weight loss, smoking cessation, metformin (to combat insulin resistance) –> metformin is often efficient to restore fertility.
The 2 exocytosis reactions after the acrosomal reaction, associated with fertilization
(1) Spermatozoan receptors bind to ZP3 causing IP3/Ca2+ increase, allowing for exocytosis of spermatozoan internal membrane contents.
(2) Spermatozoan penetration triggers increased [Ca2+]. Fusion of cortical granules from oocyte that harden glycoproteins of zona pellucida.
The same increase in [Ca2+] that triggers the cortical reaction, also triggers…
The completion of the 2nd meitotic division from metaphase II
Factors aiding in sperm transport
- estrogen primes the female tract for sperm
- cGMP gives sperm energy for movement
- decreased [H+]
- decreased viscosity of mucus
- increased ciliary and peristaltic movement and fluid flow
Effect of estrogen vs progesterone on blastocyst transport to uterus
ESTROGEN: constriction of isthmus, barring passage of embryo.
PROGESTERONE: myometrium relaxation, promoting transport of blastocyst.
3 steps of Implantation
(1) Adhesion
(2) Penetration
(3) Invasion
Adhesion
Implantation step 1
Zona pellucida dissolves (egg hatches). Il-1 critical to increase integrins for cell-cell/cell-matrix interactions. OSTEPONTIN binds integrins of endometrium and blastocyst.
Penetration
Implantation step 2
Stromal cells formed which secrete nutrients and form decidua. The serve as mechanical and immune barrier with minor endocrine function
Invasion
balance between decidual cells (defence) and trophoblast migration (offense) to allow trophoblast to enter endometrium but not too deep
Trophoblasts can differentiate into what 2 things?
(1) Syncytiotrophoblasts (most endocrine functions)
(2) Cytotrophoblasts (secrete CRH, TRH, and somatostatin)
THESE ARE THE FUNCTIONAL HORMONAL CELLS OF THE PLACENTA
HCG has what feedback effects?
High HCG has negative feedback on LH/FSH (preventing further pregnancy). Complemented by the increased inhibin during pregnancy.
HPL
Human Placental Lactogen
Produced by syncytiotrophoblasts. Stimulates lipolysis and has anti-insulin actions on maternal carbohydrate metabolism (allowing more nutrients to reach the fetus).
Estriol
Major estrogen of pregnancy. Made from DHEA that comes from fetal adrenal gland/liver. Finalized in fetal placenta.
Progesterone affect during pregnancy
Needed for establishment and sustenance of fetus. Also promotes mammogenesis (stimulates alveolar pouched of mammary glands).
What secretes Relaxin?
Corpus Luteum and later the placenta
OT and contractions
OT increases uterine contractions. Estrogen increases number of OT receptors and sensitivity increases 200 fold in early labor.
Ferguson reflex
Distension of cervix which serves as signal for OT to rapidly increase at beginning of labor
Letdown reflex
Contraction of mammary gland for milk ejection. Stimulated by OT due to baby crying/increased mammary circulation.
