Male Reproductive Physiology Flashcards
how is genetic sex determined?
by the sex chromosomes
when do the testes begin to develop in the males?
gestational weeks 6-7
when do the ovaries begin to develop in the females?
gestational week 9
how is phenotypic sex determined?
by the hormonal output of the gonads
what is puberty initiated by?
the pulsatile secretion of GnRH, which in turn drives the pulsatile secretion of FSH and LH
what does the pulsatile secretion of FSH and LH stimulate?
the secretion of the gonadal steroid hormones (testosterone and estradiol)
what happens when there are increased circulating levels of the sex steroid hormones?
they are responsible for the appearance of secondary sex characteristics at puberty
what are the two main functions of the testes?
spermatogenesis and the secretion of testosterone
what are the seminiferous tubules?
they are epithelium formed by the sertoli cells with interspersed germ cells
what is the composition of adult testis?
80% seminiferous tubules and 20% connective tissue interspersed with leydig cells
what is the function of leydig cells?
they synthesize and secrete testosterone
what are the androgens secreted by the testes?
testosterone, dihydrotestosterone (DHT), and androstenedione
what happens to most of the testosterone in the target tissues?
it is eventually converted into DHT
what do the testes lack and what does this mean?
the testes lack 21-beta hydroxylase and 11-beta hydroxylase; therefore, no glucocorticoids or mineralocorticoids are synthesized
what enzyme do the testes have and what is its purpose?
17-beta hydroxysteroid dehyrdogenase; it converts androstenedione to testosterone
what is the end product of steroid synthesis in the testes?
testosterone
how is testosterone concentrated in the lumen seminiferous tubules?
by binding to the androgen-binding protein (ABP)
in some tissues, DHT is the active androgen. What tissues are these?
prostate gland in the adult and the external male genitalia
what converts testosterone into DHT?
5-alpha reductase
what is most of the circulating testosterone bound to?
plasma proteins and albumin; plasma protein: sex-hormone-binding globulin SHBG
what does deficiency of 5-alpha-reductase lead to?
ambiguous external genitalia
where are estrogens found to have a high concentration in the male?
in the fluid of the seminiferous tubules
what is the putative source of the estrogen in the fluid of the seminiferous tubules?
the sertoli cells
how is testosterone converted to estradiol?
by the enzyme aromatase (CYP19)
what is one potential important role of the estrogen found in the fluid of the seminiferous tubules?
it has a potential important role in spermatogenesis
where are much larger amounts of estrogens formed from testosterone in other tissues of the body?
adipose tissue
what is the rate limiting step in the synthesis of testosterone?
the conversion of cholesterol to pregnenolone
what enzyme is responsible for the conversion of cholesterol into pregnenolone?
cytochrome P450 side-chain cleavage (P450SCC) enzyme
what is the primary endocrine cell of the testis?
leydig cell
where does synthesis and secretion of Testosterone occur?
in leydig cells
how do the leydig cells get cholesterol?
they can synthesize cholesterol de novo; they can also acquire it from the circulation, through LDL receptors and HDL receptors
how is free cholesterol generated within the leydig cells?
by a cholesterol hormone-sensitive lipase (HSL)
what is the action of HSL?
it converts cholesterol esters to free cholesterol for androgen production
how is cholesterol transferred within the mitochondrial membranes?
via the steroidogenic acute regulatory protein (StAR)
what is another name for the P450SCC enzyme?
cholesterol desmolase
what stimulates the conversion of cholesterol to pregnenolone and regulates the overall rate of testosterone synthesis by the Leydig cell?
LH
how does LH promote pregnenolone synthesis (2 ways)?
it increases the affinity of the P450SCC enzyme for cholesterol or it will stimulate the synthesis of the P450SCC enzyme (long-term action)
60% of the circulating testosterone is what?
bound to sex-hormone binding globulin (SHBG)
38% of the circulating testosterone is what?
bound to albumin
2% of the circulating testosterone is what?
the free testosterone- which is the biologically important form
which form of testosterone influences the HPA axis?
the free testosterone
when does testosterone become present in the embryonic life?
at the 2nd month
what effect does testosterone have on the testes during the last 2-3 months of pregnancy?
the descent of testes
what is testosterone’s actions at puberty?
increased muscle mass, pubertal growth spurt, closure of the epiphyseal plates, growth of the penis and the seminal vesicles, deepening of the voice, spermatogenesis, libido
what are the specific actions of DHT?
fetal differentiation of the external male genitalia and prostate, male hair distribution and male pattern baldness, sebaceous gland activity, and growth of the prostate
what can be used as a treatment for benign prostatic hypertrophy and hair loss in males?
5-alpha-reductase inhibitors
what are some of the classic signs and symptoms of benign prostatic hyperplasia (BPH)?
urinary frequency, urinary urgency, nocturia, difficulty initiating and maintaining a urinary stream, a feeling of postvoid fullness in the bladder, and dribbling
what are the concentrations of DHT like in the men with BPH compared to men without BPH?
they are not higher- they are actually equal
so what might cause BPH if there is not more DHT?
men with BPH may have more DHT receptors on their prostates
what type of pathway does the LH receptor on the leydig cell activate when it binds?
a cAMP-PKA pathway
what happens when LH binds to the LH receptor on the leydig cell?
it results in steroidogenesis and testosterone production
what is the sertoli cell stimulated by?
testosterone and FSH
what type of pathway does the testosterone and FSH receptor activate when testosterone/ FSH binds on the sertoli cell?
a cAMP-PKA pathway
what happens when FSH or testosterone binds to receptors on the sertoli cells?
it results in protein synthesis and the production of inhibin, ABP, aromatase
what is the effect of the production of inhibin?
it inhibits FSH release
what does binding of testosterone in the lumen of the seminiferous tubules provide?
a local testosterone supply for the developing spermatogonia
where does the aromatization of testosterone to estradiol take place?
in the sertoli cells
what produces inhibin to regulate FSH levels?
sertoli cells
which one does GnRH favor, LH or FSH? why?
GnRH favors LH over FSH becasue the sertoli cells produce inhibin which negatively feedbacks to the anterior pituitary to decrease the production of FSH
what are the three phases of spermatogenesis?
mitotic divisions, meiotic divisions, and spermiogenesis
what are the male gamete cells?
spermatids (haploid 1 N DNA)
once the first round of meiosis 1 is completed, what are these cells known as?
secondary spermatocytes (haploid 2N DNA)
what is the karyotype of the primary spermatocytes?
diploid 4N
what cells do you have after the completion of meiosis II (super fast)?
spermatids (haploid 1N)
what is the process that converts the spermatids to spermatozoa?
spermiogenesis
when talking about spermatogenesis, what happens at puberty?
the mitotic cycles are going to increase and the spermatogonia or stem cells divide to produce daughter spermatogonia
after the last division of spermatogonia, last division of mitosis, what do you have?
the primary spermatocyte
what is the general definition of meiosis?
production of the haploid gamete
what happens during the meiosis phase of spermatogenesis?
the primary spermatocytes will undergo two meiotic divisions
what does the first meiotic division produce?
it produces two secondary spermatocytes, each with a haploid number of duplicated chromosomes
what enters the second round of meiosis during spermatogenesis?
2 secondary spermatocytes
what does the second meiotic division of spermatogenesis produce?
two spermatids each (4 total), each with a haploid number of unduplicated chromosomes
where and with what does spermiogenesis end with?
it ends in the testis with the release of spermatozoa from sertoli cells
as the spermatid matures, there are going to be elements of the cytoplasm that are known as what? and what will happen to these?
they are known as residual bodies, and they will be phagocytized by sertoli cells
what is the effect of FSH on spermatogenesis?
it stimulates the Sertoli cells to nurse and form sperm- without this stimulation, spermatogenesis will not occur
what is the beginning of sperm formation and what hormone is responsible for this?
the growth and division of the testicular germinal cells is the beginning of sperm formation, and this is caused by testosterone
what happens when a person is consuming an exogenous form of testosterone or an androgenic analog?
the exogenous androgens enter the circulation and exert excessive negative feedback on the hypothalamus and pituitary (there will be insufficient spermatogenesis due to lowered intratesticular levels of T)
where does decapacitation of sperm occur?
in the epididymis
what is the function of the seminal vesicles?
they secrete a mucoid material containing nutrients as well as prostaglandins (aids in fertilization) and fibrinogen
how do prostaglandins aid in fertilization?
they react with the female cervical mucus to make it more receptive to sperm movement (make the cervical mucus less thick) they also cause backward reverse peristaltic contractions in the uterus and fallopian tubes to move the ejaculated sperm toward the ovaries
what is the function of the prostate gland?
it secretes a thin milky fluid containing Ca2+, citrate ion, phosphate ion, and a clotting enzyme; helps with pH adjustment
what is the composition of semen?
fluid and sperm from the vas deferens, fluid from the seminal vesicles, fluid from the prostate, and a small amount of fluid from the bulbourethral gland
what is the final pH of semen?
7.5
an erection can be classified as what type of event?
a neurvascular event
during the flaccid state, blood flow to the erectile tissue is?
minimal due to vasoconstriction of vasculature
what happens during an erection?
the parasympathetic nerves that innervate the vascular SM of the helicine arteries that supply the blood to the cavernous spaces release NO
what is the effect of the NO that that parasympathetic nerves release?
it activates guanyly cyclase, which increases cGMP, which causes a decrease in intracellular Ca2+ levels
what happens when there is a decrease in intracellular Ca2+ levels in the erectile tissue?
it causes relaxation of the vascular SM, so vasodilation allows blood to flow into the spaces causing engorgement and erection
what type of control is emission under?
sympathetic control (norepinephrine transmitter)
what is emission?
the movement of semen from the epididymis, vas deferens, seminal vesicles, and prostate to the ejaculatory ducts
what is ejaculation caused by?
the rhythmic contraction of the bulbospongiosus and the ischiocavernous muscles
what is the effect of testosterone deficiency in the 2nd-3rd month of gestation?
results in varying degrees of ambiguity in the male genitalia
what is the effect of testosterone deficiency in the 3rd trimester of pregnancy?
leads to problems in testicular descent along with micropenis
what is the effect of testosterone deficiency at the time of puberty?
leads to poor secondary sexual development and overall eunuchoid features
what is eunuchoidism?
persistence of prepubertal characterisitcs anf often by the presence of characteristics typical of the opposite sex
what is the effect of testosterone deficiency post-puberty?
it leads to decreased libido, erectile dysfunction, decrease facial and body hair growth, low energy, and infertility
what is Kallman’s syndrome?
a genetic disorder; occurs when GnRH neurons fail to migrate into the hypothalamus during embryonic development; it is a form of hypogonadotropic hypogonadism
what is Kallman’s syndrome characterized by?
delayed or absent puberty and an impaired sense of smell
what is klinefelter syndrome?
primary hypogonadism; individuals with 47, XXY genotype; individuals are phenotypically male because of the presence of the Y chromosome; seminiferous tubular dysgenesis
what happens at puberty in patients with klinefelter syndrome?
the increased levels of gonadotropins fail to induce normal testicular growth and spermatogenesis; the seminiferous tubules are largely destroyed, resulting in infertility
what would you expect the levels of testosterone and LH to be in a patient with klinefelter syndrome?
decreased testosterone and increase LH
what would you expect the levels of testosterone and LH an GnRH to be in a patient with Kallmann’s syndrome?
decreased GnRH, decreased LH, and decreased testosterone
what does a hyperprolactinoma (tumor in the pituitary) cause?
it suppresses FSH and LH secretion through the excess secretion of prolactin (prolactin has a negative feedback on GnRH)
what do tumors of the testis (interstitial cell tumors) produce?
large amounts of testosterone
what happens to serum LH and FSH levels as men age?
tjeu rise (FSH more so than LH)
