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Reproductive Physiology > Male Reproductive Endocrinology > Flashcards

Male Reproductive Endocrinology Flashcards

1
Q

what causes genotypic sex, gonadal sex and phenotypic sex?

A

genotypic: y chromosome
gonadal: SRY gene encodes TDF- testis transcription factor
phenotypic: hormones produced by gonads

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2
Q

what is the phenotypic sex?

A

development of accessory sex organs, external genitalia and secondary sex characteristics

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3
Q

what does SRY cause?

A

development of gonad and germ cells into testes and spermatogonia

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4
Q

what hormone causes the development of external genitalia?

A

dihydrotestosterone (DHT)

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5
Q

what causes XX males? what is the impact on gonads?

A

the SRY gene translocates to the x chromosome in crossing over
normal testis are not produced but it is still male

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6
Q

describe the surroundings of the indifferent gonad

A

it is associated with the mesonephros, the excretory (wolffian) duct and the paramesonephric (mullerian) ducts

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7
Q

what do the mesonephros, wolffian duct and mullerian ducts form in the male fetus?

A

mesonephros- epididymis
wolffian- vas deferens, seminal vesicles and ejaculatory duct
mullerian ducts degenerate

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8
Q

what to the mullerian ducts form in the female? what prevents this in the male?

A

fallopian tubes, uterus and cervix

anti mullerian hormon from sertoli cells causes degeneration

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9
Q

what do androgens produced by the leydig cells promote? which androgen is required for each?

A

differentiation of the wolffian duct (requires testosterone) and prostate development (requires DHT)

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10
Q

in the absence of testosterone, what happens to the external genetalia?

A

female structures are formed (homologies between male and female)

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11
Q

what does the hypothalamic-pituitary-testis axis regulate in males? what is the feedback mechanism?

A

spermatogenesis and androgen production

testis products inhibi hypothalamus and anterior pituitary

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12
Q

describe the release of GnRH, LH and FSH in males? what happens with constant GnRH release?

A

pulsatile

constant levels of GnRH prevent LH and FSH release by downregulating receptors

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13
Q

what is another name for kallmann syndrome? what mutations cause it?

A

hypogonadotropic hypogonadism

KAL-1, FGFR1, PROK2 and PROKR1

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14
Q

what are the two main consequences of hypogonadotropic hypogonadism?

A

anosmia (inability to smell) and lack LH and FSH

link between the developmental origin of olfactory cells and GnRH producing cells

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15
Q

what is the main danger for patients with kallmann syndrome?

A

osteoperosis- hormone replacement therapy indicated

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16
Q

what causes the proliferation of leydig cells in the prenatal stage of male development?

A

maternal chorionic gonadotropin (early development) and embryonic leutinizing hormone (late development)

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17
Q

describe the activity of the hypothalamic-pituitary-gonadal axis prior to puberty

A

few GnRH pulses with low LH and FSH levels
high negative feedback sensitivity
spermatogonia are diploid and undifferentiated in the testis

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18
Q

what 6 events happen in male puberty?

A

GnRH pulses increase (frequency and amplitude), negative feedback decrease, gonadotroph sensitivity to GnRH increases, LH and FSH production increase, testosterone increase (with spermatogenesis) and androgen changes of puberty occur

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19
Q

where are the receptors for LH? what does stimulation do?

A

Leydig cells- transcribe proteins involved in testosterone biosynthesis

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20
Q

where does FSH bind and what are the results?

A

binds to the basolateral membrane of sertoli cells stimulating transcription and synthesis of aromatase, growth factors, ABP and inhibin

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21
Q

what are the two negative feedback routs of the hypothalamic-pituitary-testicular axis?

A

1) testosterone inhibits GnRH release and LH release

2) inhibin inhibits FSH release

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22
Q

what is the effect of LH binding on Leydig cells?

A

GPCR produces cAMP and activates PKA
increases enzymes in testosterone synthesis, stimulates rate limiting step and stimulates sterol carrior protein and activating protein

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23
Q

what are the 4 primary actions of FSH?

A

on sertoli cells
increases androgen binding protein (keeps local testosterone high), P450 aromatase (produces estrogen), growth factors to support sperm productiion and inhibins that supress leydig cell proliferation and FSH secretion

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24
Q

what are the secondary effects of FSH?

A

acts on Leydig cells and increases sperm motility

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25
Q

how do Leydig cells and Sertoli cells act upon eachother?

A

L cells make testosterone- acts on S cells
S cells convert T into estradiol (aromatase)- acts on L cells
S cells generate growth factors that act on L cells

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26
Q

what is the precursor for androgen synthesis? where does the first step occur?

A

cholesterol

mitochondria

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27
Q

what is the rate limiting step of androgen synthesis and what stimulates it?

A

desmolase producing pregnenolone

up regulated by LH

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28
Q

what are the extratesticular sources of androgens?

A

adipose tissue, skin and adrenal glands

29
Q

what causes male pseudohermaphroditism?

A

any deficit in the mechanism by which androgens act in genetic males

30
Q

what is the result of 5 alpha reductase deficiency?

A

DHT levels are reduced and testosterone levels are normal- faialure of urogenital sinus and external genitalia development

31
Q

what does androgen insensitivity syndrome cause? how?

A

male pseudohermaphroditism

androgen receptors are defective- UG sinus and external genitalia are female and wolffian ducts degenerate

32
Q

what are the two types of androgen effects in the body?

A

androgenic: maturation of the sex organs and development of secondary sex characteristics
anabolic: promote protein synthesis, muscle growth and increase bone strength and length

33
Q

what causes maturation of bones indirectly in men? what is the result on bone growth?

A

estradiol metabolites- more gradual in men than women

34
Q

how do men and women’s brains compare?

A

men have a larger brain but women have more dendritic connections

35
Q

how do gonadotropins compare in males and females? what causes the difference?

A

male FSH levels are 8 times higher because of E2 (estrogen), testosterone and DHT

36
Q

why do men have a higher hematocrit than women?

A

because androgens increase expression of erythropoietin from the kidneys

37
Q

what type of receptor binds androgens and which androgen has highest affinity?

A

homodimeric receptor to direct transcription

DHT has greater activity than testosterone

38
Q

what portion of testosterone is biologically active and what percentage of total testosterone is it?

A

free in the blood- only 2%

39
Q

what is another name for andropause and what is the consequence?

A

senescence- not an abrupt loss of fertility but decrease in testosterone and quantity and quality of sperm. gonadotropins increase (mid 50s)

40
Q

when are there spikes and general increases in testosterone?

A

during fetal development, short lived increase after birth and low levels until puberty

41
Q

what are the effects of reduced testosterone?

A

decreased bone formation, muscle mass, appetite, libido and hematocrit

42
Q

what patients should be treated with testosterone therapy?

A

those with low testosterone below 300ng/dL and without prostate or breast cancer

43
Q

what does finasteride do and how? what are the side effects?

A

blocks DHT production to treat male pattern baldness

side effects: impotence, abnormal ejaculation and depression

44
Q

what can be a result of too much testosterone?

A

cause prostatic hyertrophy or cancer, causes congestive heart failure and high RBC count

45
Q

what are effects of anabolic steroid abuse?

A

reduced sperm count, testicle shrinkage, permanent heart, liver and kidney damage, psychiactric problems, breast enlargement in men and excessive body hair in women

46
Q

what are the effects of anabolic steroid use on cholesterol?

A

increases LDL and decreases HDL

47
Q

what is another name for kennedy’s disease? what is the cause?

A

spinobulbar muscular atrophy

LMN disease caused by mutation in androgen receptor by CAG repeat expansion (glutamine)

48
Q

what is the result of the mutated receptor in kennedy’s disease?

A

toxic gain of function- degeneration of motor neurons in brain stem and spinal cord. muscle wasting by middle age (onset depends on number of repeats)
some signs of reduced androgen receptor function

49
Q

describe the location of a sertoli cell and how they relate to germ cells.

A

span from basal lamina to lumen of seminiferous tubule

connected by tight junctions and surround developing germ cells.

50
Q

describe the maturity of sperm as you move through the seminiferous tubule.

A

sperm are least mature near the basal lamina and most mature near the lumen of the tubule

51
Q

at what stage does a sperm move into the lumen of the seminiferous tubule?

A

as a spermatid (after spermiation)

52
Q

what does the spermatid mature into? what dose it require and how long does this take?

A

spermatozoa
testosterone
70 days

53
Q

how are sperm activated?

A

by physiological changes in the female genital tract- become hyperactive

54
Q

what does the acrosome of the spermatozoa do?

A

it offers protection and carries enzymes necessary to dissolve the jelly coat of the egg during fertilization

55
Q

what glands produce the seminal plasmid and what is the concentration of sperm?

A

seminal vesicles, prostate gland and blubourethral glands

>20 million sperm/mL

56
Q

what does the seminal vesicle produce?

A

70% of semen volume- large amount of fructose

57
Q

what spinal segments provide the sympathetic innervation of the male genitalia and what does it cause?

A

T11-L2

responsible for emission and ejaculation. sympathetic tone maintains detumescence (sexual arousal)

58
Q

what spinal segments provide parasympathetic innervation to the male genitalia and what is it responsible for?

A

S2-S4

corporeal vasodilation and smooth muscle relaxation leading to tumescence (erection)

59
Q

where do the somatic and sensory aspects of penile control travel? what is the blood supply to the penis?

A

pudendal nerve

pudendal artery

60
Q

which sympathetic plexi and nerves contribute to the penis?

A

mesenteric, hypogastric and pelvic plexi

hypogasteric and cavernous nerves

61
Q

which parasympathetic plexi and nerves contribute to the penis?

A

pelvic plexus

pelvic nerve and cavernous nerve

62
Q

what do nerve terminals of the PNS release on the penis? what is the result?

A

acetylcholine and nitric oxide
relaxes smooth muscle by increasing cGMP (NO)
acts through M3 receptors on endothelial cells to produce more NO (ACh)

63
Q

how does viagra work?

A

inhibits cGMP- specific phosphodiesterase keeping cGMP levels high
stimulates erection only during arousal

64
Q

describe the mechanics of erection

A

PNS fibers cause dilation of arteries, decrease in sympathetic tone (increased blood flow)
striated muscle contraction causing decreased venous flow and sinusoids of corora expand causing an erection

65
Q

what veins are compressed in erection?

A

venous plexus and larger veins in the tunica albuginea

66
Q

what are the mechanics of emission?

A

movement of ejaculate into urethra- SNS cuases contraction of smooth muscle of distal epididymis, vas deferens and accessory glands

67
Q

what prevents sperm backflow?

A

internal sphincter of the bladder

68
Q

what is anejaculation and what causes it?

A

inibility to ejaculate

sexual inhibition, medication, ANS malfunction, prostatectomy and ejaculatory duct obstruction

Reproductive Physiology (6 decks)

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