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