Male Gonad Physiology Flashcards
___ stimulates leydig cells in testes to make testosterone.
LH
HPG (T) axis
hypothalmic gnrh –> anterior pituitary lh, fsh –> testosterone and inhibin in testes
___ stimulates sertoli cells in testes to promote sperm development
FSH
___ forms inhibin in testes which is a mode of negative feedback
FSH
____ feedsback at the pituitary from the testes
inhibin
____ feedsback at the pituitary and hypothalamus from the testes
testosterone
____ syndrome results from low production of gnrh in parvi-cellular hypothalamic neurons due to failure of cell precursors to migrate to the hypothalamus
kallman’s
GnRH is secreted into the ____ portal.
hypothalamo-hypophyseal
T/F GnRH levels in serum are too low for detection
T
Target of GnRH
gonadotrope cells in anterior pituitary
Circadian output of GnRH is regulated by _____ which results in highest levels of GnRH when?
melatonin –> peak in morning (highest level of LH and testosterone as well)
T/F stress and other similar changes may inhibit gonadtropin release
T
Higher frequency pulsatile gnrh release favors ___ secretion
LH
Excessively frequent pulsation/pathologic or continuous GnRH initially increases LH and FSH in a ____ effect but leads to GnRH receptor downregulation with resulting low LH/FSH. This can be mimicked by treatment with a GnRH agonist like ____
flare effect –> downregulation –> leuprolide
The process by which GnRH binding sites increase during troughs of GnRH pulses is called______
self priming
GnRH analog like leuprolide results in high/low LH
low
T/F LH and FSH are stored in separate granules
T
LH is metabolized by the ___
liver
LH/FSH has a longer serum half life.
FSH = 2 hours vs 20 mins
___ residues on FSH inhibit its metabolism
sialic acid
negative feedback on FSH is mediated by ____
inhibin b
negative feedback on lh is mediated by ____
testosterone
in early fetal development _____ controls development of testes and wolffian ducts
placental hcg
in late fetal development ____ controls testes development as fetal HPG axis matures
pituitary lh
In infancy, the hypothalamus is very sensitive to ___ negative feedback.
steroid
At what point in time do nocturnal FSH/LH pulses begin?
puberty
Testosterone synthesis
LH –> receptor –> STAR protein transports cholesterol from mitochondria into lumen of cell –> side chain cleavage to form pregnenolone –> either to progesterone or to androstenedione to testosterone
______ is the rate limiting step of steroid synthesis
transport of cholesterol out of mitochondria into cell lumen by steroidogenic acute regulatory protein (STAR)
_______ creates a hydroxyl group at the 17 carbon and cleaves the sidechain in steroid production
17 hydroxylase
The final step of steroid production involves ____ which removes a keto group to form testosterone.
17beta dehydrogenase
___ converts pregnenolone to progesterone
3beta dehydrogenase
T/F most testosterone is free in circulation.
F –> mostly bound to albumin or SHBG but 2% free for receptors
_____ binds androgen receptor with greater affinity than testosterone
DHT
What is the location of the androgen receptor?
nucleus
androgens dislodge ____ from the androgen receptor during binding
hsp90
___ is needed to stimulate sertoli cell function but ___ is the main regulator of spermatogenesis
fsh and testosterone
testosterone enters sertoli cells bound to ____
androgen binding protein
4 ways sertoli cells support spermatogenesis
create specialized microenvironment, expose germ cells to high levels of testosterone, coordinate maturation via gap junctions, and transport of differentiating germ cells toward lumen
____ occurs when anti-sperm antibodies form as a response to breach of the btb
autoimmune orchitis –> destruction of contralateral testis
Type Ad sperm stem cells do what?
undergo mitosis to maintain supply, line basal layer –> dark
Type Ap sperm stem cells do what?
undergo mitosis to produce clonal population, linked by cytoplasmic bridges –> mature simultaneously
What kind of sperm stem cells enter spermatogenesis and then spermiogenesis
Ap –> b
___ undergo meiosis 1
primary spermatocytes
____ undergo meiosis 2
secondary spermatocytes –> form spermatids
____ undergo spermiogenesis
spermatids
4 stages of spermiogenesis
golgi, cap, acrosome, maturation phases
____ phase is when a spermatid developes polarity
golgi phase
___ phase is when the spermatid nucleus condenses and forms a cap
cap phase
___ phase is when the acrosome matures and a tail develops
acrosome phase
____ phase is when excess spermatid is extruded into a residual body
maturation phase
Identification of primary hypogonadism
infertility precedes testosterone deficiency//fsh is elevated
Identification of secondary hypogonadism
same time infertility and testosterone deficiency // low fsh and lh
1st trimester hypogonadism leads to ___ and ___
ambiguous genitalia and hypospadias
2nd/3rd trimester hypogonadism leads to ___ and ___
micropenis and cryptorchidsm
Eunuchoid body proportions result from hypogonadism in what stage of life?
childhood (also pubertal delay/absence, and gynecomastia)
What are the associated hormone levels? normal men or obstruction
normal
What are the associated hormone levels? isolated spermatogenic failure
high fsh
What are the associated hormone levels? hypergonadotropic hypogonadism (aka testicular failure)
high fsh, high lh, low testosterone
What are the associated hormone levels? hypogonadtropic hypogonadism
low/normal fsh and lh, low testosterone
Most common cause of congenital primary hypogonadism
Klinefelter 47 xxy
increased risk of testicular cancer
klinefelter
Bell clapper deformity
malformation of processus vaginalis (acrquired hypogonadism)
testicular torsion and mumps orchitis can result in ____
acquired primary hypogonadism
When does gonadtropin therapy for secondary hypogonadism have best efficacy?
if onset of secondary hypogonadism occurred after puberty
