other than the common ones, what else does test do
brain - helps conc, maybe memory
increases lean muscle and cuts down fat
increases bone density and growth
3 peaks of T timings
First is pre birth = gonadal differentiation
Second is either prenatal or v soon after birth depending on species (just use term PERINATAL) and this = sexual dimorphism in brain
Main bump is third one, during puberty
mullerian duct
forms uterus
wolffian duct
forms vas deferens
what causes degradation of mullerian duct
presence of testes
secretes both androgens and anti mullerian hormone AMH
where on Y chromosome is maleness determined
Maleness is conferred by a small region at the tip of the Y
chromosome, the location of the SRY gene
sex determining region
what cells in epiblast migrate to gonadal ridge
primordial germ cells
leydig cells role
angrogen production
sertoli cells role
germ cell develpoment support
effect of sry gene expressed in male cells in early embryo in gential ridge
first sertoli cells differentiate
sends signal to steroid secreting cells to start secreting test
and therefore these convert to leydig cells d
all fucnitons of sertoli cells
-Secrete substances initiating
meiosis
-Secrete testicular fluid
-Concentrate testosterone locally
with androgen binding protein
-Release AMH, preventing
formation of a female oviduct.
-Protect spermatids from the
immune system.
-Produce lactate, the preferred
energy source of
spermatocytes/spermatids
general sperm formation pathway
spermatogonia
primary spermatocyte
secondary spermatocyte
spermatid
spermatozoa
XO
Turners syndrome
XXY
Klinefelters syndrome
test receptor name
NR3C4
effect of test vs effect of DHT
Testosterone:
Spermatogenesis
Testicular descent
Wolffian duct growth
Gonadotrophin hormone regulation
Differentiation of brain via oestrogen
5α-dihydrotestosterone:
External virilization
Maturation at puberty
what drug can cause accidental exposure to androgens and its effect
danazol
used to treat endometriosis
when given to pregnant woman - baby is genetic female but externally virilised (has a pp) and masculinised brain (maybe)
Klinefelter symptoms
XXY
Small intra-abdominal testes, low testosterone
production
Some limited breast development
No spermatozoa produced (XXY germ cells
cannot survive in testicular environment)
Scant body hair
Mullerian duct absent
Wolffian duct present
Penis developed
No cure, simply symptoms management.
Swyer symptoms
XY gonadal dysgenesis
Male karyotype, but undeveloped
Female appearance
No testicular development,
Ovaries develop, then degenerate (streak gonads)
Uterus and vagina are normal, but no menstruation
No sex steroids
No pubic hair
No breast development
Tall stature
No puberty
Infertile
High risks of gonadal cancer
Swyer treatment
HRT to induce female puberty and development of
uterus, with or without testosterone to support
gender identity, gonadectomy, ART possible
provided uterus can develop.
with Swyer, what % of cases are mutation in SRY gene
15%
rest may have mutations in genes that are nec for the response to SRY)
androgen insensitivity syndrome symproms
Lack of androgen receptor, body cannot perceive testosterone
Testicular oestrogen drives breast development.
Breasts develop well as no testosterone signal capable of
opposing oestrogen
Tall stature
No uterus present, as AMH is produced by testis
Testis do not descend as this is dependent on a testosterone
signal.
Vagina is short and blind ending
androgen insensitivity syndrome treatments
Multidisciplinary treatment depending on the individual and their
family, and depending on whether this is a partial or complete
AIS: HRT (oestrogen or testosterone), gonadectomy to prevent
tumours or surgery to “repair” male genitals (orchiopexy),
counselling
cause of 46,XX
Originate from receiving a X
chromosome from the father with the
SRY gene incorrectly attached to it, due
to crossover during meiosis in
spermatocytes/spermatids.
