Male Hormones B&B Flashcards
what are the respective functions of LH and FSH in males?
FSH stimulates spermatogenesis by the Sertoli cells of the testes
LH stimulates Leydig cells of the testes to produce testosterone
what enzyme is required to convert testosterone to dihydrotestosterone (DHT)?
5-alpha reductase converts testosterone to DHT in peripheral tissues (DHT is more potent/stable)
finasteride
5-alpha reductase inhibitor —> decreases conversion of testosterone to DHT
used to treat prostatic hyperplasia and hair loss in men
where and how is testosterone converted to estradiol in males?
aromatase converts testosterone to estradiol (17beta-estradiol) in adipose and Leydig cells
some effects of testosterone are mediated by estradiol
what hormone is required for development of external vs internal male genitalia in the fetus, respectively? from what embryonic structure are these derived?
internal genitalia are derived from mesonephric duct and require testosterone (seminal vesicles, epididymis, vas deferens)
external genitalia are derived from urogenital sinus and require DHT (penis & scrotum, but also prostate, bladder)
how does 5-alpha reductase deficiency present in males?
5-alpha reductase converts testosterone to DHT
recall internal male genitalia require testosterone, but external male genitalia require DHT
—> normal internal genitalia but female external genitalia (may be mistaken for female)
why is acne common during male puberty, PCOS, and some forms of congenital adrenal hyperplasia?
sebaceous glands contain androgen receptors, which simulate growth and secretions
these are all clinical scenarios with increased androgens
what is the cause of “male pattern balding”
aka androgenic alopecia, caused by androgens
mainly mediated by DHT (can be treated with finasteride, 5-alpha reductase inhibitor)
explain why exogenous testosterone causes a decrease in spermatogenesis
exogenous testosterone will suppress LH secretion, decreasing testosterone secretion from Leydig cells (negative feedback)
however, exogenous testosterone is weaker than endogenous, so it will not be able to induce spermatogenesis
what are the negative effects of anabolic steroids?
- increase LDL, lower HDL
- erythrocytosis (increase RBC)
- small testes (neg feedback of FSH/LH)
- azoospermia (exogenous testosterone is too weak to induce spermatogenesis)
- gynecomastia (via conversion to estradiol)
why does gynecomastia occur with spironolactone use?
spironolactone: inhibits aldosterone, K+ sparing diuretic
aldosterone has similar structure to androgens —> spironolactone can thereby also block androgen receptors
on the other hand, spironolactone can be used to treat acne, hirsutism, and alopecia (but can also cause amenorrhea)
alternative drug to spironolactone that can be used in heart failure and does NOT cause gynecomastia
eplerenone (slightly modified structure so it does not also block androgen receptors)
what is the function of Sertoli cells and by which hormones are they activated?
Sertoli cells: Support/nourish developing Spermatozoa, regulate Spermatogenesis, form blood-testis barrier
stimulated by FSH and supported by paracrine Leydig cell testosterone (which is simulated by LH)
what is the function of the following hormones secreted by Sertoli cells?
a. inhibin B
b. androgen-binding protein
c. anti-mullerian hormone
a. inhibin B: negative feedback to FSH secretion
b. androgen-binding protein: raises/maintains local testosterone levels in the testes (relative to peripheral tissue)
c. anti-mullerian hormone: results in degeneration of müllerian ducts (female structures) in fetus
Mullerian vs Wolffian duct
Mullerian aka paramesonephric duct —> develops into female genitalia
Wolffian aka mesonephric duct —> develops into male genitalia
both exist in utero initially
what occurs in complete androgen insensitivity syndrome (CAIS)?
mutation in androgen receptor in males - no cellular response to androgens, no male genitalia develops except testes which form due to presence of SRY gene
Sertoli cells (testes) still secrete MIH (Mullerian inhibitory hormone), so there are no female genitalia either
basically, baby appears female but has no internal genitalia except testes
what are the complications of cryptorchidism?
aka undescended testes (uni/bilateral) - usually in abdomen or inguinal canal, exposes Sertoli cells to higher temperature
—> low sperm count
—> low inhibin levels
—> risk of germ cell tumors
—> inguinal hernias
—> testicular torsion
what is a dangerous cause of bilateral undescended testes that should be ruled out?
congenital adrenal hyperplasia - baby could actually be a female (XX) exposed to increased androgens, resulting in ambiguous genitalia but lacking testes
dangerous because there is a risk of shock from low cortisol! Test the ACTH and cortisol levels
varicocele is a dilatation of the _____ of spermatic veins
varicocele is a dilatation of the PAMPINIFORM PLEXUS of spermatic veins
more common in the left (via “Nutcracker effect” - L spermatic vein compressed between aorta and superior mesenteric artery)
also associated with renal cell carcinoma (R spermatic vein varicocele is very uncommon, must consider this as a cause)
from which hypothalamic nucleus is GnRH secreted?
preoptic nucleus - secretes GnRH in a pulsatile manner
where are Sertoli cells found in the male reproductive tract?
Sertoli cells are found in the Seminiferous tubules and induce Spermatogenesis
FSH stimulates myoid cells (neighboring Sertoli cells) to produce _____
FSH stimulates myoid cells to produce PmodS, which in turn stimulates Sertoli cells to produce androgen-binding protein (ABP)
what are the intermediates of spermatogenesis?
- spermatogonium (2n)
- mitosis —> primary spermatocytes
- meiosis I —> secondary spermatocytes (1n)
- meiosis II —> spermatids
- spermiogenesis —> spermatozoa
when and where does capacitation vs activation of spermatozoa occur?
capacitation = terminal differentiation, occurs in epididymis pending ejaculation
activation occurs during ejaculation - hyperactivation of sperm motility
what occurs in the cortical reaction? (3)
sperm is incorporated into ooplasm, triggering:
1. hyperpolarization
2. increased Ca2+ concentration
3. cortical granule hardening of zona pellucida (prevents additional sperm entry)
