L79: Reproduction 1 Flashcards
Where is gene encoding for SHBG located?
X chromosome (think XXY Klinefelters - double the amount of SHBG, so less free T!)
Where’s the SRY gene located?
Y
When does Mieosis II resume, in the female ovary
upon fertilization
What does SRY encode for?
Testes determining factor (TDF)
Gonadal sex determination is
A. Hormone dependent
B. XX or XY dependent
B.
Germ cells are precursors for
Spermatogonia or oogonia
Coelomic epithelium is a precursor for
Sertoli cells and granulosa cells
Mesenchymal cells are precursors for
Leydig and theca cells
Leydig and theca cell origin?
Mesenchymal cell
Sertoli cells and granulosa cell progenitor?
Coelomic epithelium
In a male, the _________ develops into seminiferous tubules, spermatogonia, sertoli cells, and leydig cells
medulla
In a female, __________ develops into secondary sex cords, oogonia, theca cells, and granulosa cells
cortex
You diagnose a male patient with hypergonadotrophic hypogonadism. Which one of the following pathologies could explain the high FSH/LH with low testosterone? A. Androgen insensitivity B. Klinefelter's syndrome C. Kallman's syndrome D. Fetal pseudohermaphroditism E. Turner's syndrome
A or E
Turner’s syndrome
XO (gonadal dysgenesis) in utero, females need both X chromosomes to develop ovaries. Later on they can be inactivated as bar-bodies. Uterus with no ovary results.
Big idea: maleness is
imposed. default is feminine program.
Testosterone promotes the preservation of
A. Wolfian ducts
B. Mullerian ducts
A.
What hormone, secreted from testes, promotes the atrophy of the mullerian duct?
Anti-mullerian hormone
What enzyme makes DHT from T?
5-alpha reductase
Which is NOT formed from the Wolffian duct? A. Epididymis B. Vas Deferens C. Seminal vesicles D. Ejaculatory duct E. Leydig cells
E. Leydig cells (actually what promote preservation of Wolffian duct in the first place)
BIG IDEA: Even though the female program is default, and female structures develop with out a hormone…
…GROWTH TO NORMAL SIZE requires estrogen in the same way that development of male genitalia requires that 2nd testosterone surge at puberty.
In utero, after 9 weeks without ____ it will go ahead and make an ovary
Testes determining factor
What does finesteride (propecia) do?
blocks 5-alpha reductase
Seminiferous tubule dysgenesis
XXY klinefelters
Androgen resistance produces
male pseudohermaphroditism
male pseudohermaphroditism
female phenotype, underdeveloped female structures due to lack of estradiol, but XY genetic sex.
21 hydroxylase deficiency
congenital adrenal hyperplasia
What is the mullerian/wolffian duct status of Turner’s syndrome?
Developed Mullerian duct
Regressed Wolffian duct
What is the mullerian/wolffian duct status of an XY patient, with loss of X-linked gene for androgen receptor?
Regressed Mullerian duct
Regressed Wolffian duct
This patient has SRY, TDF, testes, and testosterone. But T receptors absent. So Wolffian duct will regress since T cannot tell it to remain. Mullerian duct will regress too, since testes is still producing AMH.
What is the mullerian/wolffian duct status of an XY patient, with deficient 5 alpha-reductase?
Regressed Mullerian duct
Developed Wolffian duct
…remember 5-alpha reductase converts T to DHT. Only T is necessary to preserve Wolffian duct not DHT. This person might have underdeveloped external genitalia or something, though
What is the mullerian/wolffian duct status of an XXY patient?
Developed Mullerian duct
Regressed Wolffian duct
Female phenotype with testes
male pseudohermaphroditism (Eg. Androgen resistant patients. No pubic/axillary hair, undescended testes)
male phenotype with ovaries
female pseudohermaphroditism
True hermaphrodite
both gonadal sexes present
Most testosterone is bound to
Cortisol Binding Globulin (55%)
45% is bound to SHBG
2% is free
What is the source of all circulating DHEA
Adrenal cortex (reticularis)
Do adrenal androgens (DHEA) influence male accessory organ development?
No.
Which is the strongest androgen? A. Testosterone B. Androstenediol C. Androsterone D. Testosterone E. Di-hydrotestosterone
E.
While only 2% of T is excreted in free form, the rest is
converted to 17-ketosteroids & DHT, conjugated into water soluble forms, then excreted.
DIRECT effects of testosterone include
- Development of epididymis, vas deferens, seminal vesicles.
- Larynx (male voice lowering)
- RBC, muscle mass, fat, bone
- Increased VLDL and LDL, decreased HDL
Male pattern baldness. Direct or indirect (DHT) effect of testosterone?
indirect (DHT)
In UTERO, DHT promotes development of A. Epidydimis B. Vas Deferens C. Seminal vesicles D. Penis
D. Penis
note: A, B and C are promoted by T in utero.
In UTERO, T promotes development of A. Penis, urethra B. Scrotum C. Prostate D. Epidydimus
D. Epidydimus (plus vas deferens, seminal vesicles)
A-C are DHT’s job in utero
In PUBERTY, T promotes development of
Penis Seminal vesicles Musculature Voice Skeleton Spermatogenesis
In PUBERTY, DHT promotes development of
Scrotum
Prostate
Male pattern bear, balding, escutcheon
Sebaceous glands
Treatment for benign prostatic hypertrophy (BHP)
5-alpha reductase inhibitor, suppress DHT thus prostate growth
Constant high levels of GnRH is
INHIBITS release of FSH and LH at anterior pituitary
Prostate cancer treatment
Androgen receptor blocker (flutamide)
Continuous GnRH agonist (shuts off LH)
Testosterone only
Liver (increase VLDL & LDL, decrease HDL) RBC Muscle mass Abdominal visceral fat Larynx (male voice) Epidydymis Vas Deferens Seminal Vesicles
DHT only
Prostate Beard Growth Sebum formation Penis Scrotum Urethra Prostate
T and DHT
Seminal vesicles
