Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endo Repro Exam 2 > Male Reproductive Physiology > Flashcards

Male Reproductive Physiology Flashcards

1
Q

what are the important time points for sex differentiation?

1) what happens during first 5 weeks
2) what happens during the 6th and 7th week for genetic males?
3) what about at week 9 if don’t have AMH and testosterone?

A

during first 5 weeks –> gonads are going to be neither male or female (bipotential)

gestational weeks during 6-7 –> testes begin to develop in genetic males

gestational week 9 the ovaries begin to develop in the absence of testosterone and AMH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the gonadotropin secretion over the lifetime? (Male an female)

1) what happens during the fetus?
2) childhood? (what is more, FSH or LH)
3) puberty?
4) what changes during adult reproductive behavior?
5) what about at senescence? what is higher and why is that the case?

A

fetus: early spike in Gonadotropin release. (one big output), and right around postnatal time.
childhood: not much in childhood, but there is more FSH than LH!!

Puberty: rising

Adult reproductive period: within the female we have a particular cyclic behavior associated with the LH surge and menstruation.. LH > FSH!!!

Senescence (menopause) –> low levels of estrogen and progesterone, which takes off the negative feedback, so even higher FSH / LH.. but FSH is back to being higher than LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Up until puberty, what’s to note about gonadotropin in males and females?

A

they have the same oscillations up until that point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does the pulsatile secretion of FSH and LH do?

clinical application of GnRH analogues?

A

stimulates secretion of gonadal steroid hormones, testosterone and esetradiol

these sex steroid hormones are responsible for secondary sex characteristics.

GnRH analogues need to be given in a pulsatile manner and very specific concentrations. if you have a long-acting one given.. puberty is not initiated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What inhibits GnRH release? (3 things)

what releases one of these and when is it released?

what are the implications of removing melatonin?

A

1) extreme stress
2) caloric deprivation in women

3) melatonin that’s released from pineal gland

melatonin levels are high during childhood and low in adulthood

if you remove the pineal gland it creates early puberty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Function of the testes?

Scrotum?

Epididymis?

A

spermatogenesis and secretion of testosterone

its lower temperature is essential for spermatogenesis –> 1-2C below body temperature

primary location for the maturation and storage of sperm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Vas Deferens function?

Seminal Vesicles?

Prostate gland?

A

provides another storage area for sperm (ampulla), secretes fluids rich in citrate and fructose

secretes fluid rich in citrate, fructose, prostaglandins, fibrinogen

secrete milky aqueous solution rich in citrate, calcium, and enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

prostaglandins from seminal vesicles? (2 things)

A

prostaglandin react with the female cervical mucus to make it more receptive to sperm movement (make cervical mucus less thick)

causes backward, reverse peristaltic contractions in the uterus and Fallopian tube to move the ejaculated sperm toward the ovaries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what kind of pH do sperm need to be more functional?

A

alkaline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the seminiferous tubules?

what 2 sperm cell types are there? and where are they located?

what are these in?

what cell type is outside of the tubules?

A

epithelium formed by the Sertoli cells, with interspersed germ cells

1) spermatogonia (progenitor cells) –> most immature germ cells.. located near the periphery of the tubule!
2) Spermatozoa (mature sperm) –>mature germ cells, located near the lumen of the tubule

all of the sperm are in Sertoli cells

Leydig cells are between seminiferous tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Leydig Cells? where are they located?

what do they produce?

A

interstitial cells that lie between the seminiferous tubules

they produce testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

function of Sertoli cells?

1) what do they do for the sperm?
2) what do they do to protect the sperm?
3) how do they help the sperm move in the seminiferous tubules?

A

1) nutrients to differentiating sperm
2) form tight junctions with each other creating a barrier between the testes and the bloodstream.. protecting for development
3) secrete fluid into the lumen of the seminiferous tubules which helps transports perm through the tubules into the epididymis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 3 main hormones the testes produce?

what are all 3 hormones collectively called?

which is most abundant?

what’s most abundant in target tissues? How?

A

testes can produce:

1) testosterone
2) dihydrotestosterone
3) androstenedione

ALL CALLED ANDROGENS

testosterone is most abundant

much of the testosterone in target tissues is converted to DHT by peripheral conversion (dihydrotestosterone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Testosterone is sythesized where?

why do the testes not create glucocorticoids or mineralcorticoids?

A

synthesized and secreted by Leydig cells of the testes

the testes do not have 21B hydroxyls or 11B hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

2 main enzymes driving testosterone synthesis? what does it do?

what is the end product of the testes?

A

they do have 17B hydroxysteroid dehydrogenase (17B-HSD) to convert androstenedione to testosterone

3B hydroxysteroid dehydrogenase –> mediating some of the precursors of testosterone

the end product is Testosterone… not DHEA and androstenedione

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what’s the concentration like of the Testosterone in the seminiferous tubules? what’s helping this do that?

what is the active testosterone hormone though?

A

T is HIGHLY concentrated by binding to androgen-binding protein (ABP)

this helps keep the concentration within the seminefirous tubules 100x higher than the blood.

Free, not the one bound to ABP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

explain the peripheral conversion of testosterone?

what converts testosterone to DHT?

A

there are some elements in development that are going to be dependent on something other than testosterone..

one is dihydrotestosterone (DHT). –> this is converted from testosterone by 5a reductase in PERIPHERAL TISSUES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

in circulation, not in the seminiferous tubules, what is testosterone bound to?

again, what’s bound in the seminiferous tubules?

A

Sex Hormone-binding globulin (SHBG)

ABP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where do leydig cells get their cholesterol from?

how is it getting into the leydig cells?

say we have it stored.. how does it go from stored to free cholesterol?

what is it converted to after it’s free cholesterol?

A

it can be synthesized or obtained from circulation from LDL or HDL.

it’ll be shuttled into the cells and into the mitochondria thanks to the sterotidogenic acute regulatory protein (StAR)

it can store cholesterol esters, and when we use more, we use hormone sensitive lipase which converts cholesterol esters to free cholesterol for androgen production

cholesterol is then converted to pregnenolone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Explain the production of estrogen in the male?

A

aromatase is produced by Sertoli cells, and aromatase which is the enzyme catalyzing testosterone to estradiol.

just knowing that males produce estrogen too

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the mitochondrial pathway of androgens?

cholesterol to pregnanalone

A

mitochondrial pathway

we have the side chain cleavage by P450SCC which removes the side chain from the carbon at position 20 of cholesterol –> pregnenalone

(this is desmolase)

it’s the Rate Limiting Step!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Pregnenalone to testosterone?

Once you get to DHEA, what are the two ways in which you go from DHEA to testosterone?

A

Pregnenalone –> 17a hydroxypregnenalone via (17a hydroxylase)…

this goes to DHEA through 17,20 desmolase (same as 17a-hydroxylase)

1) DHEA then is changed to Androstenediol through 17b- Hydroxysteroid dehydrogenase

Androstenediol can be changed to testosterone through 3b hydroxysteroid dehydrogenase

2) DHEA can be changed to AndrosteneDIONE, then to testosterone through 17B hydroxysteroid dehydrogenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What’s the precursor to DHT?

enzyme?

A

Testosterone

5a reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Precursor to Androsterone?

enzyme?

A

AndrosteneDIOL

5a reductase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Estrone?

Estradiol?

how do these two go from androstenedione and testosterone to these forms?

A

weaker form of estrogen

predominant estrogen species especially during the menstrual cycle

Aromatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does LH stimulate the synthesis of pregnenolone? (remember, cholesterol to pregnenalone requires P450scc) –> 2 things!!

what is another name for P450scc?

A

increasing affinity of P450scc enzyme for cholesterol!!

stimulates the synthesis of the P450scc enzyme (long-term action)

DESMOLASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the overall main stimulus for leydig cells to produce testosterone?

what does this stimulus do then for testosterone?

A

LH!!

they control the conversion of cholesterol to pregnenolone and the overall rate of synthesis for testosterone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

when does testosterone production begin?

A

7-8 weeks of the fetus

29
Q

How does testosterone bind to target tissues?

where are they found?

are they found only on reproductive tissue?

A

they bind to androgen receptors (AR) (along with the other androgens that the testes produce)

these are found in prostate, testis, epididymis, seminal vesicles

also found in non-repro tissue –> CNS, anterior pituitary, thyroid, skin, adrenal cortex, liver, etc.

30
Q

DHT production?

1) where does it bind?
2) this compared to testosterone, which has a greater affinity?
3) is DHT the active form? why or why not?

A

also binds to androgen receptors, but with a greater affinity than testosterone

you’d think it’s the active androgen but it’s not because the production is more limited and it’s not feeding back into the hypothalamus

it’s going to have particular functions regardless.

31
Q

if we have 5a-reductase deficiency, what’s going to happen?

A

DHT needs 5a reductase, so if we didn’t we’d have ambiguous genitalia

DHT determines external genitalia.

32
Q

what are the fates of testosterone? (like what is bound or not bound)

which one is active?

A

60% Testosterone is going to bind to SHBG in circulation

38% of it is going to be bound to albumin

2% is free is our ACTIVE.. that can feed into the axis.

33
Q

What can happen if testosterone is present or absent at the 2nd month of embryonic life?

1) at 2 months, if it’s present what do you have?
1) at 2 months, if it isn’t present what do you have?

A

at 2 month of embryonic life is important for male with XY

if you have testosterone, you get the penis and scrotum

if we lack it at that time, this can lead to the formation of clitoris and vagina

34
Q

What are the fetal actions of testosterone? (2)

what happens if the testes don’t descend, what is that called?

why isn’t external associated with testosterone?

A

differentiation of the internal male genital tract (epididymis, vas deferens, seminal vesicles)

causes descent of testes into scrotum during last 2-3 months of pregnancy

Cryptorchidism (lack of testosterone so no descent)

it kind of is, but external is by DHT

35
Q

What is the actions of testosterone at puberty?

don’t memorize, just look at it

A

increasing muscle, growth spurts, closure of the epiphyseal plates, penis and seminal vesicle growth, deepening of voice, spermatogenesis, libido

36
Q

Specific actions of DHT? (4)

1) DHT on genitalia, hair, prostate, and sweat?

A

1) differentiation of the external male genitalia.
2) male hair distribution and male pattern baldness
3) growth of the prostate
4) sebaceous gland activity

37
Q

What is the androgenic actions of testosterone and its’ friends? (3)

A

regulation of differentiation of male internal and external genitalia in fetus

stimulation of growth, development of 2ndary sexual characteristics at puberty

maintenance of repro tract and production of semen, imitation and maintenance of spermatogenesis

38
Q

Anabolic actions of androgens? (7)

1) blood?
2) what about general body structure?
3) any carrying molecules?
4) behavior?
3 more

don’t memorize, just look

A

red blood cell production

sebaceous gland secretion (DHT) *** know this one

protein anabolic effects (nitrogen retention)

linear body growth, bone growth, closure of epiphysis (through estrogen)

stimulation of ABP synthesis

Maintenance of secretion of sex glands

regulation of behavioral effects, including libido

39
Q

What is very specific to DHT actions on that web diagram? ****

What’s specific to testosterone?

Estrogen in the male?

A

penis, scrotum, urethra, prostate

Beard growth, sebum formation, prostate growth

Testosterone = voice changing, epididymis, vas deferens, seminal vesicle formation.

bone formation

40
Q

person has trouble urinating.. when it starts it stops easily.. wakes up multiple times per night.. has had UTIs over the past year.

Dx?

A

Benign Prostatic Hyperplasia

41
Q

what is Benign Prostatic Hyperplasia (BPH)?

1) symptoms?
2) DHT in prostatic tissue?
3) what probably is the cause?
4) what do you think they may prescribe then?

A

***Growth of the prostate

include urinary frequency, nocturne, difficulty imitating and maintaining a stream, feeling postpaid fullness in bladder, dribbling

men don’t have a significant elevated DHT

it’s suggested that it might be because there are more DHT receptors! so bigger prostates?

targeting. 5a reductase

42
Q

what is the intracellular mechanism of action of testosterone?

1) how do leydig cells make testosterone?
2) where can this testosterone do? what does it participate in with the Sertoli cell?
3) how do Sertoli cells create estradiol? (using one thing)
4) what else do they produce through FSH? (2 extra things)

A

LH binds on the leydig cell through a receptor

Gs is activated by LH, which leads to enzyme synthesis that are forming the synthesis of testosterone from cholesterol

Testosterone can go into the blood stream or it can go into the Sertoli cells and then it’ll be important for spermatogenesis with FSH!

FSH binds to the FSH receptor on the Sertoli cell, which will also go through a Gs pathway to increase protein synthesis.. one of which is aromatase which will help change testosterone to Estradiol

it also produces ABP for increasing testosterone in the lumen

and inhibins A and B (inhibits FSH release at the level of the pituitary)

43
Q

What specific hormone is being produced in Sertoli cells that helps the differentiation of male internal genitalia?

A

AMH

44
Q

What’s an explanation as to why we are producing more LH than FSH at puberty?

A

because Sertoli cells are making a ton of sperm, and in doing so it’s also making inhibins, which are acting on the anterior pituitary to inhibit the release of FSH

45
Q

Spermatogenesis?

A

occurs along the seminiferous tubules.

3 phases:

1) mitotic divisions
2) Meiotic Division (2 rounds)
3) spermiogenesis (conversion of the spermatids to mature sperm)

46
Q

Process of Spermatogenesis

1) what’s the first germ cell
2) what do you get when you have spermatogonia? 2 types
3) what goes into meiosis?
4) what goes through meiosis 1?

5)

A

Primordial Germ Cell –> Spermatogonium (2N DNA) –> 4N DNA –> Spermatogonia

2 types: A and B.

A = isn’t going to commit to meiosis.. it’s going to keep making more germ cells. this is the reservoir

B = the one that after several rounds of mitosis is going to go through meiosis.

those spermatogonia that have gone into meiosis 1 are called “primary spermatocytes” (4N)

once they finish with meiosis 1, they’re going to be called secondary spermatocytes (2N)

meiosis 2 happens quickly from secondary spermatocytes and they become spermatids (haploid, 1N)

then the conversion of rounded spermatid to the elongated flagellated spermatozoa.

47
Q

dumbed down spermatogenesis again?

A

spermatogonia –> mitosis –> last division –> 1 primary spermatocytes –> meiosis 1 –> two secondary spermatocyte –> meiosis 2 –> two spermatids –> mature to spermatozoa

48
Q

where does spermatogenesis happen?

A

seminiferous epithelium in the Sertoli cells

49
Q

What is the last part from spermatid to spermatozoa?

what happens? (3 things)

A

Spermiogenesis

1) appearance of acrosome –> creates hydrolytic enzyme for penetration of the eggs
2) development of the axoneme from the centriole that leads to the flagellum
3) reduction of cytoplasm through a “residual body” which is going to be phagocytized by Sertoli cells

50
Q

What happens in the middle piece of the sperm?

A

tons of mitochondria for the movement of the flagella

51
Q

without FSH, what should you know for spermiogenesis?

A

spermiogenesis will not occur because FSH acts on the Sertoli cells and this plus testosterone is needed for maturation.

52
Q

What is the feedback regulation of spermatogenesis?

A

in order for spermatogenesis to occur, the 100x concentration in the seminiferous tubules helps keep it.

if we change that, it’s affected.

53
Q

what happens if you had exogenous androgens being administered?

A

exogenous androgens have an impact on the axis.

you’ll have a decrease in LH and FSH but the decrease in LH is going to decrease in intratesticular levels of testosterone, which is going to be insufficient to do spermatogenesis in the Sertoli cell.

it’s also going to down regulate the hypothalamus and pituitary because of the exogenous androgen.

54
Q

What happens for sperm maturation of epidydymis?

A

sperm are less motile in the epididymis, but upon exiting they’re strongly motile.

There’s going to be a process that prevent the sperm cell from being motile and preventing the early decapacitation.

preventing early acrosome reactions before getting to the egg.

55
Q

When is testosterone levels higher in the fetus? what about neonatal?

when does testosterone and sperm production ramp up?

A

2nd trimester it’s highest!

right after birth

puberty into adulthood, and it maintains a high pace up until senescence.

56
Q

What does clotting enzyme and PSA do from the prostate?

A

helps for the liquification of the semen.

57
Q

Semen final pH? why is this the way it is?

what would consider someone infertile?

A

7.5

this is to neutralize the mild acidity of the other semen components.

anything less than 20 million sperm cells in an ejaculation is considered infertile

58
Q

Erection?

1) What’s produced first because of parasympathetics?
2) what does it lead to? include the mechanism
3) how does relaxation (election) aborted?
4) what drugs help with this?

A

neuromuscular event

parasympathetic nerves innervating the vascular SM leading to the production of nitric oxide.. this is going to lead to the relaxation of the helicine arteries, leading to the engorgement/erection

NO will act on guanylyl cyclase which changes GTP to cGMP

cGMP leads to relaxation (erection).

erections can be aborted thanks to Type 5 PDE inhibitors which change it back to GMP.. which would lose your erection.. this is why we use viagra.

59
Q

What happens when you change GTP to cGMP in the penis?

A

relaxation happens –>

increased blood Flow goes into the sinusoidal cavernous spaces

constriction around the muscle around the base of the penis leads to the –>
collapse of venous return from cavernous spaces.. leads to the full erection

60
Q

How does emission happen?

1) what kind of control?
2) what does it cause?
3) what does it try to prevent?

A

for emission there’s sympathetic control which is causing the peristaltic contraction of SM of the vas deferens

closes the internal sphincter of the bladder to prevent the retrograde ejaculation of semen into the bladder

61
Q

what happens if we destroy the internal sphincter of the bladder through a prostatectomy?

A

retrograde ejaculation

62
Q

Ejaculation?

1) what muscles are contracted during this?

A

significant somatic motor system where we have rhythmic contraction of bulbospongiosus and the ischiocavernous muscles (striated) which surround the base of the penis.

rapid exit of semen

innervated by somatic motor nerves

63
Q

Capacitation of spermatozoa and what’s going on in the female? (3)

1) what happens in the fallopian tube
2) what happens on the acrosome?
3) what about the membrane of the sperm itself?

A

**pretty much there are changes that occur in the female to allow for

the uterine an Fallopian tube wash away the inhibitory factors

loss of cholesterol that had built up on the acrosome, which makes the head of the sperm weaker

membrane of the sperm is much more permeable to Ca2+, increasing the motility of the sperm.

64
Q

Acrosome reaction?

what two enzymes are there and what do they do?

A

large quantities of hyaluronidase and proteolytic enzymes are stored in the acrosomal head of the sperm…

Hyaluronidase depolymerizes hyaluronic acid polymers in the intracellular cement that holds the ovarian granulosa cells together.

proteolytic enzymes digest proteins in the structural elements of tissue cells that adhere to the ovum

65
Q

T deficiency in 2nd - 3rd month?

3rd trimester of pregnancy?

Puberty

post puberty?

A

different degrees in ambiguity

cryptorchidism and micropenis

poor secondary sexual development and eunuchoid features

decreased libido, erectile dysfunction, decrease facial and body hair, low energy and infertility

66
Q

Eunuchoidism?

A

persistence of prepubertal characteristics

67
Q

Kallman’s Syndrome?

what is it caused by?

what do you see lower levels of?

what is the hallmark?

A

hypogonadism

GnRH neurons fail to migrate to the hypothalamus during embryonic development

so lowering production of testosterone, estrogen, and DHT

    • delayed or absent puberty
    • impaired sense of smell
68
Q

Klinefelter syndrome?

what is the cause?

what genotype?

what happens at puberty?

clinical presentation?

how do we know this is a primary disease

A

Seminiferous tubular dysgenesis

Males have an extra X, so XXY

born = male

puberty = increased gonadotropin because you have a decrease in testicular growth and spermatogenesis

**no muscle, small testes, higher gonadotropin levels but NO SPERM.

androgen production = low but GnRH and FSH/LH is high, which makes it a primary

69
Q

Tumor in the pituitary affecting gonadotropin?

A

lower LH and FSH

secondary hypogonadism

Endo Repro Exam 2 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions