W2 Male Factor Infertility & Spermatogenesis (Joey) Flashcards
Be very familiar with the HPG axis
Slide 3
FSH to Sertoli cells and helps spermatogeneis
Produce inhibin which goes back up and acts as a NFL to anterior pituitary and hypothalamus (estradiol and prolactin also have this NFL)
Sperm cell and anatomy… just for reference. Read over
Spermatogenesis
Slide 6 just read over
Which is SNS and which is PNS?
Ejaculation
Peeing
Erection
Internal urethral sphincter, part of bladder neck, part of the prostatic urethra.
It closes during ejaculation to prevent sperm entering bladder and urine doesn’t mix with sperm
Ejaculation is SNS (shoot)
Peeing is PNS
Erection is PNS (point)
Male factor infertility definition
“Inability to initiate a pregnancy after 1 year of unprotected intercourse (where all female factors have been worked up and cleared as contributory cause)”
Causes of male factor infertility
(Most are obvious)
Which of the causes is a/w alpha blocker use?
● Testosterone Deficiency / Hypogonadism - see all causes
● ED → inability to successfully copulate
● Testicular Trauma (may lead to development of self anti-sperm antibodies, obstruction)
● Obstruction in the ejaculatory tract
○ Stricture of urethra, prostatic urethra, ejaculatory ducts, etc.
○ Radical prostatectomy involves removal of the ejaculatory ducts as well, vas scars down (acts as free vasectomy) — cannot impregnant
● Ejaculatory Dysfunction:
○ Retrograde Ejaculation, alpha blockers can cause this (expulsion of semen into the urinary bladder - highly correlated with use of alpha blockers, pelvic trauma, lower motor neuron lesion - think spinal trauma may lead to decreased sympathetic tone below level of lesion, inability to appropriately innervate pelvic floor, ex inability to appropriately contract internal urethral sphincter durign ejacualtion)
● Congenital Bilateral Absence of the Vas Deferens (CBAVD)
○ Highly common in males with cystic fibrosis - nearly all CF patients have this condition. Vas deferens is gone by the time of birth. You are infertile basically
○ Early forms of the VD forms in most males with CF, but due to abnormal Cl- channels, the VD’s tracts often
cannot fully form/mature, of if they do, it collapses → the VD’s luminal endothelium adheres together → scars
down → long-term obstruction
○ T levels usually normal, but patient has azoospermia / severe oligospermia
Patient work up is basically the same
Infertility — treatment options
What are the two medications
What should you not do as a treatment?
Slide 13
—weight loss
Hormonal optimization” - goals are boosting FSH and making T wnl if low
○ May offer the patient the following, but these are “off-label” (not FDA approved for use in men)
■ Clomid - a selective estrogen receptor modulators (SERM) that acts centrally to partial antagonize central E2 receptors ( why do this? )
=LH and FSH will increase — increase T and sperm counts
■ Anastrozole, letrozole - Aromatase Inhibitors, may decrease peripheral conversion of T → E2 somewhat → decreased negative feedback loop response → increased gonadotropin release, hopefully increased sperm counts and improved sperm quality. Decreasing estrogen negative feedback so increasing LH and FSH
○ May NOT treat infertility with traditional testosterone replacement - higher physiologic levels of T lead to increased negative feedback loop which leads to HPT axis suppression → infertility
If not helpful, referral to reproductive urologist +/- endocrinology