Male Reproductive System (McCumbee and Richardson) Flashcards
Kartagener Syndrome
Pts. have immotile cilia and are infertile
Spermatogonial proliferation
Spermatogonia divide mitotically to renew stem cells and expand the differentiating spermatogonia
*Differentiating spermatogonia undergo incomplete cytokinesis leaving intracellular bridges for the transport of molecules b/w cells
Spermatogonial meiosis
During prophase, homologous chromosomes pair and are held together by the synaptonemal complex which facilitates recombination; remnant of this is the chiasmata
First division => Homologous pairs separate (2C); is now a secondary spermatocyte
Second division => Sister chromatids separate (1C); are now four haploid spermatids
Spermiogenesis (Spermy-spermy-grow-grow)
- Chromatin is inactivated via condensation by protamines; replaces the Histones in chromatin
- Excess cytoplasm is collected into the residual body and digested by Sertoli cells
- Acrosome cap is formed and contains hyaluronidase, acrosin, neuraminidase, and acid phosphates
Phases of acrosomal cap formation
- Golgi- Pro-acrosomal granules bud from the Golgi complex and fuse to the anterior membrane
- Cap & Acrosomal- Vesicle spreads over surface
- Maturation- Assumes characteristic shape
Flagellum Formation
Part of spermy-spermy-grow-grow that involves the migration of centrioles near the membrane and are arranged in a 9+2 arrangement
*Occurs @ same time as acrosomal cap formation
Factors that impair spermy-spermy-grow-grow
Irradiation
Excess steroid hormones
Elevated temperature
Vitamin A deficiency
Ducts
Intratesticular: Tubuli recti and rete testis
Extratesticular: Efferent ducts, epididymis, vas deferens, urethra
*Sperm gain motility during storage in the epididymis
Sperm cycle stages
One cycle= Amount off time to make it thru all 6 stages
*16 days
Maturation of Sperm= 4 cycles X 16 days = 64 days
*Are developed asynchronously along the tubule to release sperm continuously
Structure of Sperm
Head- Contains haploid nucleus and acrosomal cap
Mid-piece- Contains axoneme, mitochondrial sheath, and outer dense fibers
Principal piece- Contains axoneme, outer dense fibers, and fibrous sheath
End piece- Contains ONLY axoneme
Bioavailable testosterone
Free testosterone+ Testosterone-albumin
-Is only weakly bound to albumin
LH Receptor
Stimulation causes increased cAMP
=> Increased StAR, Increased P450cc, and Increased 17a-hyrdoxylase
5a-reductase inhibitors
Used to treat prostatic cancer
*Enzyme normally forms the metabolically hyperactive dihydrotestosterone
Aromatase in males
Primarily found in adipose, CNS nuclei, and some Leydig/Sertoli cells
*Converts testosterone to estradiol
Primary stimulus for Leydig cell development
hCG
Testosterone/Sperm production in male lifespan
Neonate- High
Childhood- Random surge but normally low
Adolescence- Increasing
Adult- Highest
Elder- Steady decrease
*Also a steady increase in SHBG
Androgen actions in the adult
- Promote vocal cord thickening (deeper voice)
- Promote EPO secretion (increased Hcrt)
- Promote bone growth and resorption (also closure of epiphyseal plate)
- Promote hair growth
- Promote protein anabolism
Blood-testis barrier
Formed by tight jnxns b/w Sertoli cells; prevents the development of autoantibodies against sperm
*Are connected to developing germ cells via gap jnxns
ABP
Secreted by Sertoli cells when stimulated by FSH or testosterone; helps to keep testosterone levels elevated in the seminiferous tubules
AMH receptor mechanism
Two threonine kinase receptors will dimerize after AMH binding and phosphorylate Smad 3
=> NLS is activated and Smad3 combines w/ Smad4 when it enters the nucleus and activates transcription of genes promoting apoptosis
Inhibin B
Blocks GnRH stimulated release of FSH @ the gonadotrope (adenohypophysis)
- Production is stimulated by FSH and testosterone to provide negative feedback
- Has NO EFFECT on LH release
Endocrine regulation of spermatogenesis
Pituitary: FSH => Increased Sertoli fnxn (growth factors for sperm, ABP, Inhibins)
LH => Produce testosterone to assist Sertoli fnxn
- Testosterone will activate genes, produce some estradiol, and promote ABP production
- Intact hypothalamic-pituitary-gonadal system required for all of this
Events in epididymis
Sperm become motile and are decapacitated
*Spend a month here
GnRH secretion
Must be in a pulsatile fashion to promote spermy-spermy-grow-grow
*Continuous release results in a fnxnal castration
HPG axis control
Pre-pubescent: Under CNS inhibition
Puberty: Increased LH surges @ night
Decreased negative feedback inhibition of testosterone
Increased GnRH pulses and increased sensitivity
=>Increased FSH and LH
Helicine Arteries
Supply the cavernous spaces of the penis; are constricted in the flaccid state
Erectile Response
Lower tactile stimulus or psychic stimulation leads to the release of NO and VIP; occurs via the pudendal or corticospinal tract respectively
=> Dilation of helicine arteries increases blood flow and compressed the venous outflow
Viagra action
Acts on PDE5 which breaks down cGMP
*cGMP is formed by guanylyl cyclase and promotes vasodilation and boners
Emission
Sympathetic neurons reach the accessory glands via the hypogastric nerve and release NER on a2-drenergic receptors
=> rhythmic contractions of smooth muscle to move semen
*Also prevents retrograde movement into the bladder by closing the internal urethral sphincter
Ejaculation
Filling of the urethra sends afferent signals via the pudendal nerve which responds w/ wavelike contractions of the bulbospongiosus to eject the load
Gynecomastia
Estrogens stimulate the growth of the female breasts (prior to growth there is no difference); could also occur w/ exposure to excess PRL
Kallman’s Syndrome
A type of tertiary hypogonadism caused by deficient production of GnRH
- testes will have arrested spermy-spermy-grow-grow and androgen deficiencies (decreased muscles, pubic hair, high-pitched voice, infantile genitali)
- Caused by a failure of the GnRH secreting cells to migrate from the olfactory placode => Anosmia
TGF-B Family
“Transforming Growth Factor”
Includes Inhibins, activins, and AMH; all secreted by Sertoli cells
Treatment of Klinefelter’s
Androgen replacement therapy can restore some secondary sexual characteristics and reverse gynecomastia but cannot induce spermatogenesis
-Due to hyalinization of the seminiferous tubules
