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BECOM II Exam 4 > Reproductive Physiology > Flashcards

Reproductive Physiology Flashcards

1
Q

Leydig cells

A

sex hormone producing cells in the testes

  • receptors for LH
  • produce testosterone
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2
Q

GnRH effect

A

stimulate gonadotrophs in ant. pituitary to release FSH, LH

  • GnRH located in arcuate and medial prepoptic areas of neurons
  • limbic system and behavior influence on production
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3
Q

LH in males

A

target Leydig cells

-stimulate testes to release testosterone

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4
Q

FSH in males

A

target Sertoli cells

-stimulate testes to produce sperm

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5
Q

aromatase

A

enzyme in sertoli granulosa cells for the converting testosterone to estrogen

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6
Q

GnRH pulsatility

A
  • short half life –> rapid degradation once released
  • pulsatile secretion needed for synthesis and secretion
  • long half life –> suppression of LH, FSH
  • G protein –> activate IP3 and DAG
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7
Q

How are the GnRH receptors regulated by downstream steroid hormones (estrogen, progesterone, test)?

A
  • regulation of the upstream (afferent) neurons that feed the GnRH neurons (indirect)
  • afferent neurons = kisspeptin
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8
Q

regulation of GnRH by upstream neurons

A
  1. kisspeptin = activated by AVPV, inhibited by arcuate
    - AVPV - GnRH release
    - arcuate - GnRH inhibitor
  2. B-endorphin = act on opiate receptors; inhibit GnRH
  3. neurokinin = stimulate release of GnRH
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9
Q

function of Kisspeptin neuron types

A

depends on estrogen levels

  • low dose estrogen –> arcuate –> inhibit GnRH
  • high dose estrogen –> AVPV –> stimulate GnRH
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10
Q

which androgens regulate GnRH pulsatility?

A

testosterone directly

  • also dihydrotestosterone (DHT)
  • testosterone prevents progesterones inhibitory effect of GnRH –> overproduction of GnRH and androgens
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11
Q

role of prolactin in males

A
  • suppress GnRH and LH

- need moderate amount - too high/low –> infertility

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12
Q

effect of stress on GnRH secretion

A

CRH, ADH, ACTH, NE, Epi –> inhibits GnRH release

-inhibiting CRH –> increase GnRH

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13
Q

role of naloxone

A

block GnRH, LH suppression by CRH –> increase GnRH

-CRH acts like beta endorphins

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14
Q

3 hormones that contain common alpha chain

A

-LH, FSH, TSH

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15
Q

how do you increase the half life of FSH, LH?

A

glycosylation (adding sugar)

  • increase glycosylation –> slower degradation of FSH, LH
  • FSH longer half life than LH
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16
Q

how do you treat prostate cancer or prevent precocious puberty?

A

give GnRH analog

  • continuous (sustained) stimulation of GnRH receptor releasing GnRH at high levels –> shut down FSH, LH
  • lost pulsatility effect for gonadotropin synthesis
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17
Q

GnRH frequency effect on FSH, LH production

A

high frequency of GnRH secretion –> increase LH, not FSH

low frequency of GnRH secretion –> increase FSH, not LH

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18
Q

regulation of GnRH in males

A
  • testosterone = inhibits GnRH and LH, FSH receptors on secreting cells
  • activin = activates FSH secretion
  • inibin (sertoli) = inhibit FSH secretion
  • follistatin (sertoli) = inactivates activin
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19
Q

role of melatonin on GnRH secretion

A

released at night and suppresses GnRH

-supplements can help prevent precocious puberty

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20
Q

Gonadotropin (FSH, LH) signaling

A

LHR, FSHR (GPCRs)

  • activate cAMP, PKA, gene transcription
  • activate Ca++ influx and Ca++ dependent kinases
  • activate PLC, IP3, DAG
  • activate PKC and COX2 –> increase prostaglandins (suppression through NSAIDs)
  • regulate own receptors by endocytosis of receptors
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21
Q

role of cholesterol in steroidogenesis

A
  • either made by Leydig fat cells or bind to cholesterol receptors
  • brought into mitochondria by STARD1
  • cleaved to pregnenolone by CYP11A1
  • adrenal insufficiency w/ STARD1 or CYP11A1 mutations
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22
Q

CYP11A1 (side chain cleavage)

A

-converts cholesterol to pregnenolone

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23
Q

CYP19A1 (aromatase)

A

-converts androgens to estrogens

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24
Q

estrogen forms

A
  • estradiol (E2) = most active

- estrone (E1) = most prominent post-menopause

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25
Q

5alpha-reductase enzyme

A

converts testosterone to dihydrotestosterone

-inhibition for prostate cancer patients to reduce dihydrotestosterone levels

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26
Q

Type I 17betaHSD

A

convert estrone to estradiol (active)

  • weak to strong estrogen
  • inactive to active
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27
Q

Type 2 17betaHSD

A

convert active androgens and estrogens to inactive

-strong to weak

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28
Q

Type 3 17betaHSD

A

convert weak androgens to strong androgens

-no conversion of estrogens

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29
Q

how can testosterone mediate its effects?

A

either indirectly or through conversion to estrogen or dihydrotestosterone
-ex. need epiphysis closure in bones through estrogen

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30
Q

how does testosterone lead to male development?

A

acts on Sertoli cells –> secrete AMH –> regress mullerian ducts and stimulate wolffian ducts

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31
Q

what 2 hormones are needed for proper spermatogenesis?

A

testosterone (stimulated by LH) and FSH

  • both act on Sertoli cells
  • estrogen also necessary for sperm maturation
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32
Q

what are the effects of elevated testosterone in blood?

A

suppress GnRH and FSH through negative feedback –> suppress spermatogenesis (infertility)

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33
Q

hypergonadotropic hypogonadism

A

high LH, FSH but low gonadal functions

-mutation in LHR or FSHR

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34
Q

hypogonadotropic hypogonadism

A

no gonadotropins (LH, FSH)

  • Sheehan’s and Kallmann’s
  • reduced steroids, spermatogenesis or both
  • caused by lesion in HPG axis
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35
Q

Sheehan’s disease

A

involution and necrosis of anterior pituitary

-no FSH, LH –> small gonads

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36
Q

Kallmann’s disease

A

failure of GnRH neurons to migrate to hypothalamus

  • no GnRH, LH, or FSH
  • no problem with development before birth (hCG dependent)
  • problem with puberty (LH, FSH dependent)
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37
Q

testicular feminization

A

body does not respond to testosterone - no androgen receptor

  • become female
  • XY female
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38
Q

Sertoli cell functions

A
  • nourish sperm during spermatogenesis
  • convert testosterone to estrogen for sperm maturation
  • form immune privileged site to protect spermatogenic cells
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39
Q

Del Castillo syndrome

A

born with Sertoli cells only

-no spermatogenic cells

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40
Q

heat regulation of testes

A
  • optimal temp for spermatogenesis
  • kept away from body (pelvis and abdomen too hot)
  • pampiniform plexus
  • cremasteric muscle in scrotum
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41
Q

pampiniform plexus

A

counter current heat exchanger

-blood in pampiniform veins cools the blood in the testicular artery

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42
Q

function of acrosome

A

contains proteolytic enzymes used to penetrate the ovum for fertilization
-provided help from prostasomes in prostate

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43
Q

functions of Sertoli cells

A
  • seminiferous fluid = flush out sperm from epididymis
  • secrete ABP = [] testosterone in testes
  • release inhibin, follastatin, activin
  • convert testosterone to estradiol by aromatase
  • contain FSH receptors
  • blood testis barrier
  • nourishment to sperm cells
  • secrete AMH = regress mullerian ducts
  • spermeation = plasminogen cut binding of spermatogonia and Sertoli cells to flush out sperm
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44
Q

when can antisperm antibodies attack sperm

A

when the female has antibodies against the sperm

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45
Q

sexual intercourse

A

PNS - erection - vasodilation by NO

SNS - ejaculation - spinal reflex (paraplegic can still get erection)

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46
Q

infertility vs. impotence

A
  • infertility = no sperm being made

- impotence = inability to have erection (PRL, damage to PNS, diabetes)

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47
Q

how do you treat erectile dysfunction?

A

give phosphodiesterase (PDE5) inhibitors to prolong the half life of cGMP

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48
Q

epididymis and ductus deferens

A
  • store and concentrate sperm

- increase mobility and fertility before ejaculation

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49
Q

seminal vesicles

A
  • provide semen
  • fructose for energy
  • prostaglandins for motility and cervix softening
  • secrete fibrinogen
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50
Q

prostate gland

A
  • secrete alkaline fluid to neutralize vagina
  • clotting and unclotting factors to hold sperm then allow it to swim freely
  • PSA good biomarker for cancer
  • prostasomes help in ovum penetration
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51
Q

capacitation of sperm

A

make sperm motile in female

-estrogen and progesterone play a role

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52
Q

role of estrogen in female

A
  • ova maturation and release
  • secondary female sex characteristics
  • transport of sperm to oviduct for fertilization
  • breast development
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53
Q

role progesterone in female

A
  • preparing environment to nourish embryo/fetus

- helps breast produce milk

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54
Q

What does GnRH –> FSH, LH stimulation release from target organ in female?

A

estrogen & progesterone

-both have negative feedback on ant. pituitary and hypothalamus

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55
Q

oogonia before ovulation in females?

A

-begin 1st part of meiotic division at the end of fetal life forming primary oocyte –> remain in meiotic arrest until ovulation

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56
Q

folliculogenesis

A

development of follicles

  • strongest one survives, all others die
  • combination of oocyte, granulosa cells, theca cells
57
Q

when is the 1st meiotic division completed?

A

during ovulation - need LH surge

58
Q

when does the 2nd meiotic division occur?

A

during fertilization by sperm

59
Q

primordial follicle

A

primary oocyte surrounded by flat (pregranulosa) cells

-conversion to primary follicles do not require hormones

60
Q

primary follicle

A

primary oocyte surrounded by cuboidal (granulosa) cells

-granulosa cells become cuboidal & form zona pellucida

61
Q

role of PRL on ovarian cycle

A

suppresses GnRH inhibiting menstrual cycle

62
Q

follicular phase in ovarian cycle

A

follicle grows/matures

63
Q

luteal phase in ovarian cycle

A

corpus luteum (formed from rupture of follicle)

64
Q

what is the clear zone b/w granulosa cells and oocyte?

A

zona pellucida which envelopes the egg

  • hardens as egg is fertilized to prevent polyspermy
  • prevents immune attack against sperm
65
Q

secondary follicular stage

A
  • proliferation of granulosa cells
  • gonadotropin dependent - FSH for follicle maturation
  • stromal (interstitial) cells form theca –> interna/externa
66
Q

role of theca interna cells

A

secrete androgen

-converted to estrogen by granulosa cells

67
Q

role of granulosa cells

A

respond to FSH to make more estrogen

-aromatase enzyme to convert androgen to estrogen

68
Q

role of testosterone and androstenedione in theca cells

A

move to granulosa cells and converted to estrogen by aromatase

  • testosterone –> Estradiol (E2)
  • androstenedione –> Estrone (E1)
69
Q

what hormone do theca cells respond to?

A

LH

70
Q

what hormone do granulosa cells respond to?

A

FSH initially

  • both FSH and LH later on
  • no FSH –> no folliculogenesis
  • FSH also increases aromatase
71
Q

what can too many theca cells lead to?

A

excess androgens –> granulosa cells cannot convert to estrogens –> androgens enter blood shutting down the negative feedback from estrogen and progesterone –> more LH release –> more androgen production
-HIRSUITISM

72
Q

what does excess testosterone for a prolonged time in females lead to?

A

converted to DHT by 5alpha-reductase

  • DHT shuts down aromatase leading to excess androgens in blood
  • seen in polycystic ovaries
73
Q

tertiary follicular stage

A
  • theca cells expand
  • fluid filled sacs (antrum) to house hormones
  • form Graafian follicle
  • higher amount of fluid –> selected to be ovulated bc it has more nutrition and hormones
74
Q

what happens with decreased blood supply to ovarian follicle?

A

atresia (degeneration of follicle)

-not enough gonadotropins

75
Q

estrogen level effects

A

high level –> GnRH release through AVPV

low level –> inhibit GnRH release through arcuate

76
Q

effects of LH surge

A

caused by high estrogen levels

  • stimulates kisspeptin
  • increase collagenase (breaks cells apart)
  • causes oocyte to finish meiosis I
  • increase muscle contraction, progesterone, luteinization
  • increase prostaglandin and histamine to increase vascularization and blood supply
77
Q

which follicles are selected for ovulation?

A

-one with the best blood supply and gonadotropin receptors (accumulate more FSH, LH)
-higher aromatase
-

78
Q

what does high dihydrotestosterone (DHT) indicate?

A
  • high testosterone and deficiency in aromatase

- death signal for follicles causing atresia

79
Q

what allows the follicle to undergo ovulation?

A

-collagenase breaks down collagen and plasminogen breaks down fibrin –> disperse theca and granulosa cells through rupture making it easier for ovulation

80
Q

function of LH surge

A

maturation of dominant follicle to resume meiosis and activate proteolytic enzymes and prostaglandins
-causes ovulation

81
Q

luteal phase

A
  • last 14 days of cycle
  • old follicular cells form corpus luteum which (maintains pregnancy)
  • no fertilization or implantation of ovum –> luteum degenerates forming corpora albicans
82
Q

corpus luteum

A
  • needed to maintain pregnancy
  • secrete progesterone for decidualization of endometrium and maintenance; also secrete estrogen
  • no fertilization –> shut down LH, FSH through negative feedback on GnRH –> shut down corpus luteum
83
Q

function of hCG

A

keeps corpus luteum alive during pregnancy by binding to same receptors as LH –> keep producing testosterone and progesterone

84
Q

what leads to the LH, FSH surge?

A

excessive levels of estradiol –> stimulate kisspeptin to increase GnRH levels through AVPV –> increase LH, FSH levels

85
Q

why are FSH levels slightly elevated at the beginning of the menstrual cycle?

A

to increase aromatase for conversion of testosterone to estrogen

86
Q

Why is there a drop in estrogen levels after the LH, FSH surge?

A

internalization of LH, FSH receptors –> less binding

87
Q

when is the 1st day of the uterine cycle?

A

during 1st day of menstruation (menstrual phase)

  • bleeding caused by collapse of endometrium in absence of progesterone and estrogen –> due to degradation of corpus luteum
  • FSH elevated due to no negative feedback
88
Q

proliferative phase of uterine cycle (1st half)

A

endometrium back to normal due to estrogen –> proliferation of endometrial cells

89
Q

secretory phase of uterine cycle (2nd half)

A

uterus development under effect of high levels of progesterone

90
Q

function of fibrinolysin during menstrual cycle

A

prevent blood clotting during bleeding

-heavy cycle (bleeding) –> not enough fibrinolysin to prevent clotting –> have blood clots

91
Q

role of prostaglandins during menstrual phase?

A

needed for contraction of uterus to prevent heavy bleeding

  • do not give NSAIDs to someone in menstrual phase
  • also helps expel blood and endometrial debris from uterus
92
Q

proliferative phase

A
  • estrogen increases proliferation of endometrial lining and increases receptors for progesterone
  • LH surge by kisspeptin stimulation –> ovulation
93
Q

secretory phase

A
  • occurs after ovulation
  • corpus luteum secretes estrone and progesterone
  • decrease uterine contractions
  • endometrium secretes glycogen
  • no fertilization –> ischemic phase –> degenerate corpus luteum
94
Q

effects of progesterone during secretory phase

A
  1. help endometrium secrete glycogen for nutrition
  2. make endometrium softer
  3. antagonizes estrogen –> prevent uterine contractions that expel things by relaxing smooth muscle
95
Q

what happens to progesterone and estrogen levels when reaching full term?

A

progesterone declines and estrogen increases –> allows for smooth muscle contraction to expel baby

96
Q

estrogen and progesterone effect on oviduct

A
  • estrogen increases motility of oviduct

- progesterone relaxes smooth muscle allowing implantation of zygote

97
Q

why is there an increased risk of osteoporosis for post-menopausal women?

A

estrogen helps prevent osteoclast activity

-more bone breakdown without estrogen

98
Q

estrogen and progesterone effect on aldosterone

A
  • estrogen –> aldosterone mimic –> Na++ and water retention
  • progesterone –> aldosterone antagonist
99
Q

estrogen and progesterone role on cervical mucous plug

A
  • estrogen = thins mucous plug allowing sperm to enter easier
  • progesterone = thickens mucous plug preventing sperm and microbes from entering (protective effect)
  • progesterone contraception to prevent fertilization
100
Q

how does oral contraception prevent ovulation?

A

contains modified estrogen (long lasting) –> inhibits GnRH, LH, FSH –> no folliculogenesis or pregnancy
-suppresses LH surge

101
Q

how does the morning after pill prevent pregnancy?

A

progesterone antagonist –> cannot maintain pregnancy leading to miscarriages

102
Q

menopause effects

A

triggered by hypothalamic changes or ovarian failure

  • higher risk of cardiovascular disease & osteoporosis
  • hot flashes due to absence of estrogen –> cannot regulate hypothalamus
  • high gonadotropins (FSH mainly)
103
Q

why are females less susceptible to cardiovascular disease?

A

estrogen and progesterone have a protective effect

-increased risk in menopause

104
Q

E1, E2, E3 dependent on age

A
  • E2 most active during reproductive age
  • E1 most active in post-menopausal women
  • E3 most active during pregnancy
105
Q

what is estrogen mostly bound to?

A

higher affinity for SHBG, lower affinity for albumin

-more albumin so more estrogen bound by albumin

106
Q

what does progesterone bind to?

A

corticosteroid-binding protein

-metabolized to pregnanediol which can be used as a marker for ovulation

107
Q

causes of female infertility

A
  1. PCOS
    - caused by high androgens and insulin resistance
    - testosterone blocks negative feedback –> stimulate GnRH –> high TSH, LH
    - treat with androgen antagonists or contraceptives
  2. hypogonadotropism
  3. hyperprolactinemia
108
Q

where is the site of fertilization?

A

ampulla of the oviduct

-ovulated egg only lasts 24 hr before it degrades

109
Q

how does female reproductive tract help in sperm migration?

A
  • contract uterus to propel sperm toward oviduct

- progesterone relaxes ovarian ducts for zygote to pass

110
Q

capacitation

A

activates sperm making it more motile

-occurs by Ca++ influx

111
Q

role of protasomes

A

help sperm penetrate zona pellucida for fertilization

-added to acrosome during ejaculation

112
Q

process of fertilization

A
  1. acrosomal reaction = sperm binds zona pellucida releasing acrosomal contents
  2. sperm pulled into ovum
    - completes 2nd meiotic division
  3. sperm and egg fuse –> zygote
113
Q

zona reaction

A

Ca++ causes cortical granules be exocytosed changing the structure of the membrane –> prevents polyspermy

114
Q

how does blastocyst implant into endometrial lining?

A

enzymes released from trophoblasts digesting endometrium –> carves holes for implantation and embryo used endometrium for nutrition

115
Q

significance of embryo being enclosed by zona pellucida

A

physical and immunological protection from mother

116
Q

Decidualization

A

uses progesterone to make endometrium softer for implantation

117
Q

role of chorionic villi

A

secrete hCG during development

-placenta provides hCG for the corpus luteum the 1st few weeks of development

118
Q

why does fetal blood have higher affinity for O2?

A

high Hb concentration and contains fetal Hb

119
Q

How do you get the conversion to estriol, the most abundant estrogen during pregnancy?

A
  1. placenta produces estrogen and progesterone
  2. progesterone reaches fetus through umbilical cord
  3. fetus makes DHEA and cortisol
  4. DHEA goes back to placenta to convert to estriol (E3) by aromatase to maintain pregnancy
120
Q

role of fetal cortisol

A
  • lung maturation

- decreases progesterone and increases estrogen for smooth muscle contraction to expel baby

121
Q

what type of estrogen is most common during pregnancy?

A

estriol (E3) coming from fetal DHEA

-maintains pregnancy

122
Q

how does high levels of progesterone lead to respiratory alkalosis?

A

increase respiratory centers –> blow off CO2 –> release more bicarb in urine to compensate

123
Q

hCG

A
  • maintains corpus luteum during the 1st few weeks bc aren’t producing estrogen and progesterone by placenta yet
  • inhibits uterine contractions (like progesterone)
  • increases thyroid hormones (like TSH)
  • declines at 10-12 weeks bc placenta is making own estrogen and progesterone
124
Q

human chorionic somatomammotropin (human placental lactogen)

A
  • hybrid b/w GH and PRL

- acts like GH on metabolism –> increase mother sugar level

125
Q

estriol (E3)

A
  • weakest estrogen
  • formed from DHEA from fetus
  • breast & duct growth, proliferate uterine muscles, increase oxytocin receptors and gap junctions
  • contract uterus if no progesterone present
  • aldosterone mimic –> HTN
126
Q

placental progesterone

A
  • maintains pregnancy
  • prevents contraction of uterus
  • inhibits milk secretion
  • converted into fetal DHEA and cortisol due to lack of 3betaHSD
127
Q

the role of fetal cortisol

A
  • at the end of pregnancy, suppresses progesterone and increases estrogen synthesis for uterine contractions
  • formed by placental progesterone
  • development of fetal lungs
  • assist milk secretion after birth
128
Q

role of fetal oxytocin

A

myometrium contraptions during labor and contraction to eject milk during lactation

129
Q

what happens to thyroid hormone levels during pregnancy

A

hCG acts like TSH and increases total thyroid hormones (T3,T4, Tg)

130
Q

fetal DHEA

A

formed from placental progesterone

-used by placenta to make estriol

131
Q

why can’t maternal cortisol enter placenta the 1st 6 months?

A

11betaHSD2 converts it to cortisone (inactive form)

132
Q

ACTH

A

acts on fetal adrenal gland for development

-stimulate fetal cortisol and DHEA release

133
Q

CRH

A

increased before birth due to fetal stress signals

-fetus head pushing against cervix –> increase CRH and ACTH

134
Q

fetal insulin

A

increased in response to high maternal glucose

-oversized fetus in uncontrolled diabetic mothers

135
Q

Parturition (labor, birth)

A
  • dilation of cervix –> increase oxytocin for uterine contractions
  • increase estrogen levels –> increase oxytocin receptors and gap junctions
  • fetal stress signals
136
Q

fetal stress signals during parturition

A

fetal stress signals –> increase CRH, ACTH –> increase cortisol release –> labor, increase milk secretion

137
Q

oxytocin during parturition & lactation

A
  • uterine contractions in labor (+ feedback)
  • expel placenta
  • stop bleeding
  • milk ejection (contract myoepithelial cells)
138
Q

stages of labor

A
  1. cervical dilation
  2. delivery of baby
  3. delivery of placenta

uterus shrinks to pregestational size

139
Q

lactation

A
  • high estrogen, progesterone –> develop breast ducts, alveoli
  • milk synthesis by PRL - inhibited by progesterone until birth
  • milk ejection by oxytocin
  • expel placenta –> steroid withdraw –> lactation
  • sucking –> increase oxytocin and PRL

BECOM II Exam 4 (10 decks)

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