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Physiology > Unit 7 - Male Reproductive Endocrinology > Flashcards

Unit 7 - Male Reproductive Endocrinology Flashcards

1
Q

male genotypic VS gonadal VS phenotypic sex

A

genotypic - Y Xm makes male
gonadal - SRY in Y Xm encodes testis determining factor (TDF) transcription factor (presence in gonad turns into testes)
phenotypic - hormones made in testes make phenotypic sex (development of accessory sex organs, external genitalia, and secondary sex characteristics)

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2
Q

what is the XX male?

A

SRY gene translocates to X Xm during male meiosis

  • ovum getting this X Xm with SRY gene develops into a male (1:100,00 births)
  • normal testes never made
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3
Q

what is the XY female?

A

similar to XX male, but if sperm carries the Y Xm that lacks the SRY gene (no TDF)
-result is XY person that looks female

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4
Q

primordial gonad

A

contains germ cells

  • the genotype of germ cells determines fate of gonad
  • considered indifferent before it differentiates into testes or ovary
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5
Q

what makes androgens and what do they do?

A

made by Leydig cells, and prmoote:

  • differentiation of Wolffian (mesonephric) duct
  • prostate (DHT only), epididymis, VDs, seminal vesicles, ejaculatory duct (testosterone)
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6
Q

what makes anti-Mullerian hormone and what does it do?

A

made by Sertoli cells and causes female Mullerian ducts to degenerate

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7
Q

how does the prostate develop?

A

series of endodermal buds located proximal to urethrea

-needs DHT

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8
Q

transformation of genital ducts in males

A
  1. when gonad is indifferent, it’s closely associated with mesonephros and excretory duct (mesonephric or Wolffian) that lead from mesonephros to urogenital sinus
    - parallel to Wolffian are paramesonephric/Mullerian ducts, that merge caudally to form uterovaginal primordium
  2. in males, mesonephros develop into epididymis, and Wolffian into VDs, seminal vesicles, and ejaculatory duct
    - Mullerian degenerate (but in females, would make fallopian tubes, uterus, and cervix)
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9
Q

what is DHT needed for?

A

make external genitalia (penis, scrotum, urethra) and prostate

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10
Q

how does the hypothalamic-pituitary-gonadal axis work in males generally?

A

regulates spermatogenesis and androgen production

  • GnRH stimulation is pulsatile, causing pulsatile LH and FSH
  • constant levels of GnRH prevent LH and FSH release (used to treat prostate cancer to lower testosterone production)
  • products of testes (mainly sex hormones and inhibin) have negative feedback on hypothalamus and anterior pituitary
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11
Q

how does the hypothalamic-pituitary-gonadal axis work in the prenatal stage?

A

Leydig cells make up more than half the testes by 60 days gestation, and are the source of sex steroid production
-increase is dependent on hCG (early development) or embryonic LH (late development)

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12
Q

how does the hypothalamic-pituitary-gonadal axis work prior to puberty?

A

few GnRH pulses, and low FSH and LH levels

  • hypothalamus and pituitary are very sensitive to negative feedback inhibition by androgens
  • spermatogonia exist in diploid, undifferentiated form in basal compartment of testes
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13
Q

how does the hypothalamic-pituitary-gonadal axis work in puberty?

A

frequency and amplitude of GnRH pulses increase, so sensitivity of HP axis to negative feedback of testosterone decreases

  • gonadotroph sensitivity to GnRH increases
  • LH and FSH production increases
  • testosterone increases and spermatogenesis starts
  • androgen-driven changes characteristic of puberty occur
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14
Q

what hormones act on Sertoli and Leydig cells? what are their hormone products?

A

FSH and LH from anterior pituitary act on Sertoli and Leydig cells respectively

  • inhibin from Sertoli negatively feedback to AP
  • testosterone from Leydig negatively feedback to AP and hypothalamus
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15
Q

what does LH do on Leydig cells?

A

stimulates GPCR to make cAMP and activate PKA to increase transcription of:

  • enzymes involved in testosterone synthesis
  • stimulates rate-limiting step (chol –> preg)
  • sterol carrier PRO and sterol activating PRO (also in testosterone synthesis)
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16
Q

what does FSH do on Sertoli cells?

A

stimulates GPCR to increase AC to increase cAMP to activate PKA to increase transcription of:

  • androgen binding PRO (keep local testosterone levels high)
  • P450 aromatase (make estrogen)
  • growth factors (support production of sperm)
  • inhibins (suppress Leydig cell proliferation)
  • factors that act on Leydig cells
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17
Q

what kind of secondary effects does FSH have?

A

on Leydig cells and sperm (increase motility)

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18
Q

crosstalk between Leydig and Sertoli cells

A
  • Leydig make testosterone that acts on Sertoli cells, which convert to estrogen to act on Leydig cells
  • Leydig also make beta-endorphins, which inhibit Sertoli cell proliferation
  • Sertoli makes growth factors to increase LH receptors on Leydig
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19
Q

what is Kallmann syndrome? main danger?

A

hypogonadotropic hypogonadism

  • development of both olfactory cells and GnRH-making cells is the olfactory epithelium (latter migrates to brain)
  • mutations in KAL-1 (X-linked), FGFR1 (autosomal dominant), and PROK(R)2 prevent neurosensory neurons from extending axons into brain, thus preventing migration of GnRN neurons into hypothalamus
  • main danger is osteoporosis, so treat with hormone replacement therapy (b/c also have little/no sexual maturation)
20
Q

rate limiting step of androgen synthesis

A

desmolase (regulated by LH) in mitochondria of Leydig cells

-removes side chain from cholesterol to make pregnenolone

21
Q

what does aromatase do and where?

A

converts androstenedione to estrone, or testosterone to estradiol in Sertoli cells

22
Q

what does 5 alpha reductase do and where?

A

converts testosterone (made in Leydig cells, moved to Sertoli) to DHT in peripheral tissue

23
Q

how much testosterone and DHT do the testes make? where else are androgens made?

A

95% of testosterone, but only minor fraction of DHT

-also made in adipose, skin, and adrenals

24
Q

what are 2 causes of male pseudohermaphroditism?

A

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

  1. 5 alpha reductase deficiency
    - DHT levels reduced, testosterone levels OK
    - failure in DHT-dependent development (urogenital sinus and external genitalia)
  2. androgen insensitivity syndrome
    - normal levels of testosterone and DHT, but androgen receptors are absent/defective
    - urogenital sinus and external genitalia develop female, Wolffian ducts degenerate, but AMH is normal to suppress Mullerian development so look female, but are sterile
25
Q

what are androgen’s actions divided into?

A

affect nearly every tissue in body

  1. androgenic - maturation of sex organs (especially penis)
    - develop secondary sex characteristics (deep voice, beard, and axillary hair)
  2. anabolic - promote PRO synthesis and growth of tissues expressing androgen receptors
    - growth of muscle and increase in strength
    - increase in bone density and strength, linear growth and maturation
    - -males have larger hearts, lungs, liver, RBCs, etc.
    - -bone maturation occurs indirectly through estradiol metabolites, and is more gradual in men than women
    - -men have larger brain, but women have more dendritic connections
26
Q

do men or women have higher FSH?

A

men have 8x higher FSH levels

-regulated by combined action of E2, T, and DHT

27
Q

androgen receptors

A

free form of testosterone is active, and enters cells by diffusion (only 2% is free; usually bound by sex hormone binding globulin and albumin)

  • binds homodimeric receptor (AR/AR)
  • directs transcriptional activity of target genes
  • DHT binds the same receptor with greater activity
28
Q

senescence (andropause)

A

testosterone decreases with age (especially ~40 years; 30% experience by mid-50’s)

  • begins to fall by 10%/year starting in 30s
  • quantity and quality of sperm decrease
  • FSH and LH levels increase
  • unlike menopause, no abrupt loss of fertility
  • causes decreased bone formation, muscle mass, appetite, libido, Hct
29
Q

effects of low testosterone

A

small percentage of men have levels <300 ng/dL

  • low sex drive, erectile dysfunction, loss of muscle mass, mood problems, fatigue, sleep disturbances, loss of body/facial hair
  • most will benefit from testosterone treatment, but not if have prostate or breast cancer
  • -can worsen sleep apnea, worsen BPH and CHF, or cause erythrocytosis
30
Q

what does Finasteride (Propecia) do?

A

block production of DHT (used to treat male pattern baldness) by blocking 5 alpha reductase
-side effects include impotence, abnormal ejaculation, and depression

31
Q

effects of anabolic steroid abuse

A
  • reduced sperm count, shrinkage of testes (b/c negative feedback causes decreased LH, so less T made in testes)
  • permandent damage to heart, liver, kidneys, psychiatric problems
  • increase LDL and decrease HDL
  • irreversible breast enlargement in men
  • excessive body hair and deep voice in women
32
Q

what is Kennedy’s disease (spinobulbar muscular atrophy)?

A

X-linked lower motor neuron disease caused by mutation in androgen receptor

  • expansion of CAG repeat in gene causes polyglutamine expansion in androgen receptor, causing toxic gain of function (onset related to size of expansion)
  • patients have progressive weakness due to degeneration of motor neurons in brain stem of spinal cord, but rarely causes death
  • early signs are weakness of tongue and mouth muscles, fasciculations, and progressive weakness of limbs
33
Q

interaction of Sertoli cells and sperm

A

spermatogenesis initiated at puberty through FSH and LH

  • single Sertoli spans from basal lamina to lumen of seminiferous tubule
  • adjacent Sertoli connected by tight junctions (barrier to prevent toxins from interfering with spermatogenesis) and surround developing germ cells
  • from basal lamina to lumen of tubule, gradual maturation of germ cells occurs
34
Q

when does spermatogenesis start?

A

at puberty by FSH via Sertoli cells

  • further supported by LH driven increases in testosterone and Sertoli cell growth factors
  • ~120 million/day
35
Q

sperm maturation

A

after spermiation, spermatids move passively into rete testes and epididymis

  • testosterone-dependent maturation needed for fully mobile/fertile sperm (~70 days)
  • after ejaculated, undergo several physiological changes in female genital tract to activate for fertilization
  • during capacitation, they become hyperactive
  • acrosome provides protection and carries enzymes for acrosomal reaction that dissolves jelly coat of egg during fertilization
  • mitochondria provide energy for swimming
36
Q

seminal fluid production

A

by male accessory glands (only 10% is sperm, so >20 million sperm/L)

  • contains sugars and ions from seminal vesicles, prostate, and bulbourethral glands
  • -seminal vesicles provide 70% volume and fructose
37
Q

where do sympathetic fibers arise and what do they do?

A

T11-L2 segments of spinal cord

  • reach genitals via mesenteric, hypogastric, and pelvic plexi, and hypogastric and cavernous nerves
  • responsible for emission, ejaculation, and detumescence (flaccid state)
38
Q

where do parasympathetic fibers arise and what do they do?

A

S2-S4 segments of spinal cord

  • travel via pelvic nerve to pelvic plexus
  • post-ganglionic fibers reach penile corpora and vasculature via cavernous nerves
  • responsible for corporeal vasodilation and corporeal smooth muscle relaxation leading to tumescence (erection)
39
Q

somatic fibers to penis?

A

travel via pudendal nerve to striated muscles

40
Q

sensory fibers to penis?

A

afferent fibers carried in dorsal nerve of penis, which reaches spinal cord via pudendal nerve, compression of which (like biking) causes temporary sexual dysfunction

41
Q

vascular components of penis?

A

pudendal artery

42
Q

how is NO related to erection?

A

nerve terminals release ACh and NO

  • ACh acts through M3 receptors on endothelial cells to make NO as well
  • NO relaxes smooth muscles, causing vasodilation of arteries, and increases intracellular cGMP levels
  • decrease in sympathetic tone allows relaxation of corpora
43
Q

what does Sildenafil (Viagra) do?

A

treats erectile dysfunction by inhibiting cGMP-specific phosphodiesterase 5 to keep cGMP levels high

  • stimulates erection only during sexual arousal
  • side effects cause blue vision, and if taken with other vasodilators will cause sudden death
44
Q

mechanics of erection

A

parasympathetic fibers in cavernous nerve cause dilation of arteriolar smooth muscle

  • decrease in sympathetic tone to vascular smooth muscle
  • increased blood flow to corpora
  • increased somatic fiber stimulation causes striated muscle contraction, causing decreased venous outflow (to keep blood engorged)
  • sinusoids of corpora expand to cause erection
45
Q

mechanics of emission

A

movement of ejaculate into urethra

  • sympathetic stimulation of hypogastric nerve causes contraction of smooth muscle of distal epididymis, VDs, and accessory glands
  • semen propelled into prostatic urethra
  • internal sphincter of bladder prevents retrograde flow of sperm
46
Q

mechanics of ejaculation

A

rapid spinal reflex expulsion of semen from urethra

  • stimulated by entry of semen into bulbous urethra
  • response mediated by spinal regions S2-S4 and somatic motor fibers of pudendal nerve
  • initiates rhythmic contractions of striated muscles of perineal area (ischiocavernosus, bulbospongiosus)
  • followed by refractory period
47
Q

anejaculation

A

pathological inability to ejaculate due to:

  • sexual inhibition
  • pharmalogical inhibition
  • ANS malfunction
  • prostatectomy
  • ejaculatory duct obstruction

Physiology (60 decks)

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