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Endocrinology > reproduction > Flashcards

reproduction Flashcards

1
Q

parts of the uterine tube

A

fundus, isthmus, ampulla, infundibulum, fimbria

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2
Q

what does the ovary contain?

A

stomal matrix, smooth muscle fibres, follicles, corpora lutea, corpora albicans and surface epithelium

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3
Q

3 week development of gonad

A

origin of primordial germ cells

route of migration- PGC migrate to genital ridges

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4
Q

4 week development of gonad

A

mesonephric ridge

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5
Q

5 week development of gonad

A

the indifferent gonad- location of primitive sex chords and primitive cords start to proliferate out. these are closely alligned to urinary system.
Male- formation of testicular capsule
female- primitive sex chords only stay in that region

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6
Q

7 week development of male gonad

A

primitive sex chords proliferate into medulla; establish contact with mesoneprhic tubule; formation of testicular capsule

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7
Q

7 week development of female gonad

A

primitive sex chords only in cortical region; medullary cords degenerate

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8
Q

20-24 week development of male gonad

A

formation of seminiferous cords connected to the mesonephric cords and wolffian duct

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9
Q

20-24 week development of female gonad

A

cortical epithelial cells enclose germ cells to form cysts –> primordial follicles

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10
Q

follicle

A

cells within follicle produce steroids

folliculogenesis accompanies and supports oogenesis

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11
Q

regulators of primordial to preantral follicle

A

primary- early antral follicle the growth is gonadotrophin independent
intraovarian / paracrine growth factors and cytokines are important
anti mullerian hormone (AMH) produced by granulosa cells of larger follicles and inhibits the primordial follicle recruitment
LIF and Kit-ligand promote primordial follicle growth
antral follicle

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12
Q

after ovulation what happens to the follicle?

A

regression of the follicle to produce the corpus luteum and release progesterone to maintain pregnancy

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13
Q

cells in primordial follicle

A

oocyte and squamous granulosa cells

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14
Q

cells in preantral follicle

A

cuboidal granulosa cells, membrane propria, theca cells for steroidalgenesis and stroma

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15
Q

cells in early antral follicle

A

accumulation of fluid in the granulosa
theca differentiates into the interna (steroid) and externa (protective)
basement membrane separates interior (avascular) from blood vessels

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16
Q

cells in the late antral follicle

A

antrum filled with fluid
granulosa thins out
cumulus- granulosa that surrounds the oocyte
still have basement membrane separating the two layers
LH surge causes these changes
enlarged antral cavity with folicular fluid
gap junctions connect follicle cells to each other and oocyte

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17
Q

oogenesis stage in the primordial follicle

A

before birth = mitosis and beginning of meiosis I (primary oocyte arrested in prophase I)
infant / child = primary oocyte arrested in prophase I

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18
Q

oogenesis stage in the primary - antral follicle

A

primary oocyte arrested in prophase I

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19
Q

oogenesis stage in the preovulatory mature follicle

A

meiosis I completed- haploid secondary oocyte

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20
Q

oogenesis stage in the ovulated follicle

A

secondary oocyte arrested in metaphase II

meiosis II is only completed if fertilised

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21
Q

what do Amh KO studies show?

A

primordials grow prematurely and depletion of primordial pool much earlier

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22
Q

regulators of early antral and beyond

A

gonadotrophin dependent- FSh and LH
granulosa and theca cells acquire FSHR and LHR
inhibin- activin - follistatin axis

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23
Q

follicular phase

A

estrogen dominance

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24
Q

luteal phase

A

progesterone dominance to support pregnancy

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25
Q

GnRH release

A

pulsatile release from the hypothalamus

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26
Q

LH and FSH release and their targets

A

LH to the theca cells (periphery) and have more access to blood
FSH release to granulosa cells

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27
Q

feedback in the hypothalamic-pituitary-gonadal axis

A

the granulosa cells produce peptide hormones inhibins and activins which feedback to anterior pituitary for FSH production

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28
Q

relationship between GnRH pulse rate and production of FSh or LH

A

pulse = high release of LH and FSH

continuous stream = decrease in hormones

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29
Q

activitin

A

increases FSH binding and FSH induced aromatisation (estrogen)
participates in androgen synthesis, enhancing action of LH in the ovary

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30
Q

follistatin

A

inhibites FSH release

bidning and bioneutralisation of activin- not directly to anterior pituitary

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31
Q

inhibin

A

supresses FSH

reduced by GnRH and enhanced by IGF-1

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32
Q

2 cell 2 gonadotrophin hypothesis - early antral follicles

A

cholesterol enters the theca cells from the blood. in the presence of LH these are converted to androgen.
androgens from theca cells enter the granulosa cells. in the presence of FSH they produce estrogen which further stimulates granulosa cell proliferation

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33
Q

role of androgens in the early antral follicle

A

substrates for the conversion to estrogens
act with FSH to stimulate granulosa cell proliferation and increase follicle size
stimulate aromatase activity this promoting estrogen synthesis

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34
Q

2 cell 2 gonadotrophin hypothesis- late antral

A

increased estrogen acts with FSH to stmulate LHR expression on granulosa cells but NOT cumululs cells
also increases LH pulses from the pituitary
LH surge—> increased production of progesterone
granulosa cells convert cholesterol into progesterone in the presence of LH

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35
Q

actions of estrogen

A

egg maturation and release
growth and maintenance of female reproductive tract
stimulates granulosa cell proliferation, which leads to follicle maturation
thins cervical mucous to permit sperm penetration
stimulates upwards contractions of the uterus and oviduct
growth of endometrium and myometrium
induces synthesis of endometrial progesterone receptors

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36
Q

role of progesterone

A

prepares a suitable environment for nourishmtne of a developing embryo/fetus
promotes formation of a thick mucous plug in cervical canal
inhibits hypothalamic GnRH and gonadotrophin secretion

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37
Q

transports of ovarian steroid hormone in plasma

A

steroids are hydrophobic and require transport molecules
once unbound can freely diffuse into cell and bind to receptors
binding proteins = albumin, sex hormone binding globulin

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38
Q

FSH and LH throughout the female life course

A

baby = higher FSh than LH

reproductive years = higher Lh than FSH

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39
Q

ovulation requires the coordination of many events

A

gene expression regulated by progesterone receptor
require vascular remodelling to increase permeability
proteases become active- model ECM
smooth muscle contraction - thinning of the wall
COC expansion- allows the oocyte to complete maturation
cumular cells adopt adhesive and migratory behaviour in response to LH
inflammatory response- why vascular remodelling is important

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40
Q

smooth muscle contraction and apical wall thinning

A

less granulosa cells along the wall
smooth muscle contractions allow layer to be broken down by proteases
EDN2 produced by granulosa cells- diffuses into theca layer where smooth muscle cells are found (externa). they contract and protude follicle forward

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41
Q

follicle wall structural changes from preantral to preovulatory

A

antral has large granulosa layers
have avariety of ECM proteins- collagen, laminin and fibronectin
lost basement membrane in the preovuatory
most surface epithelium is sloughed away
less granulosa- egg now has access to ECM proteins

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42
Q

proteolytic activity in the preovulatory follicle

A

produced from granulosa or invading immune cells
allow invagination of theca cells into follicle and provide nutrients from blood supply
include matrix metallo proteinases (MMPs), plasminogen activators, cathepsin L, ADAMTS1

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43
Q

which protease KO models don’t ovulate?

A

ADAMTS1
required for structural remodelling of the basal region of preovulatory follicles/theca invagination
KO= no invagination, basement membane remains intact
regulated by progesterone

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44
Q

ADAMTS1

A

progesterone receptor

link between this recepetor and remodelling of ECM

45
Q

cumulus expansion

A

LH surge initiates an intrafollicular signalling cascade which converge on cumulus cells via GCs
EGF-like ligans most important for expansion
cumular cells are pushed out away from oocyte- lose connection
HA strands produced by cumular cells and form matrix

46
Q

versican

A

substrate for ADAMTS1 to cells can move further away

47
Q

oocyte secreted factors

A

GDF9, BMP15
acts on SMAD2/3 and MAPK to increase oocyte quality and increase embryo development and fetal viability
bidirectional signalling betwen oocyte and follicle cells
regulate cumular cell function
transzonal projections (gap junctions) connect CCs to oocyte via zona pellucida; also CC-CC
cAMP inhibits meiosis
cGMP stops enzyme from breaking down cAMP

48
Q

LH and cumular cells

A

breakdown in connections between cumular cells and oocyte

decrease in cAMP and cGMP wihtin oocyte and therefore resumption of meiosis

49
Q

resumption of meiosis in the preovulatory oocyte

A

arrested in MII
decrease in cAMP and meoisis resumes to form a haploid secondary oocyte and is arrested in metaphse II until fertilisation

50
Q

COC activation

A

treat with LH and cumular cells have projection and move away
granulosa cells dont become migratory only cumular cells
closer to ovulation increases their abiliyt to migrate
after ovulation decreases their ability to migrate
unexpanded COC dont bind to membrane very well

51
Q

vascular remodelling

A

early follicles don’t need vascular remodelling, as factors they requires diffuse in from small capillaries in the ovary
large follicles need vascularisation remodelling to supply them with what they need for growth
angiogenesis and blood flow peak during ovulation and luteinisation
factors such as VEGF are produced by granulosa cells to increase vascular growth and permability via VEGFR-2 allows the factors to get in

52
Q

immune cell infilitration and activation in oocyte

A

increased vasodilation and permeability due to histamine and mast cells
may immune cell types in follicle
get in because basement membrane is getting broken down
driven by prostagladnins from PTGS2 in granulosa cells due to LH surge

53
Q

2 isoforms of progesterone receptor

A

PGRA in ovary

PGRB in uterus

54
Q

PGR

A

exerts pleiotrophic control over many reproductive processes
- neuroendocrine gonadotrophin regulation
uterine decidualisation
mammary galnd development
ovulation

55
Q

PRLACZ mouse

A

LacZ reporter gene into promoter region of PGR

56
Q

PGR expression

A

higly expressed in granulosa cells
transiently expressed to do with ovulation
only in mural granulosa cells, not in cumular cells

57
Q

PGR KO mouse

A

anovulatory

defect in release - oocytes are trapped in the follicle

58
Q

PGR regulated genes in the ovary

A

ADAMTS1 is essential for remodelling of the follicle wall

defects in cumulus expansion

59
Q

ovarian transplant experiment

A

PGR within ovary is important regulatory for ovulation
- WT ovary in WT ovary = normal
- KO ovary in WT ovary = didn’t restore function at all, no ovulation
- KO transplant mated to WT produced no pups
WT ovary mated to WT male produced pups

60
Q

PCOS

A

disrupted cycle and ovulation
polycystic ovaries- follicles develop to late antral phase, then arrest
hyperandrogensism

61
Q

androgens and PCOS

A

androgen excess

62
Q

experiment androgens and PCOS

A

four treatments
prenatal DHT (doesn’t convert to estrogen)
postnatal DHT
postnatal DHEA (precursor to androgens)
letrozole (prevents androgen to estrogen)

post natal DHT condition has the most traits simialr to PCOS and arrested follicles

63
Q

Androgen Receptor KO models to determine role of AR

A

use flox and cre

causes subfertility, dysfunctional ovulation, abnormal folliclar development and defective neuroendocrine control

64
Q

does androgen excess initate the development of PCOS via intra or extra ovarian AR-mediated mechanisms?

A

extra-ovarian - brain specific loss of AR signalling
intra-ovarian - granulose cell specific loss of AR signalling
if PCOS is not observed then AR signalling is required
therfore AR signalling within the brain, not ovary is a major mediator in PCOS development

65
Q

testic migration during development

A

10-15 weeks - pelvic position, suspensory ligaments and regresses
25-28 weeks- migrates over pubic bone , reaches scrotum by 35-40 weeks

66
Q

cremaster muscle

A

allows the sac to be withdrawn closer or further away

67
Q

dartos muscle

A

wrinkles skin on scortum and decreases SA to control temperature

68
Q

structure of testis

A

highly convoluted tubules to increase SA and increase sperm production
covered by thick connective tissue capsule - tunica albuginea
rete testis- labyrinth of tubules within mediastinum, drains to the head of the epididymis via efferent ductules

69
Q

functional compartments of testis

A

intratubular compartment

  • contains the sertoli cells
  • sperm production
  • seminiferous tubules

peritubular compartment

  • neuronal and vascular elements
  • leydig cells
  • steroid production
70
Q

adult seminiferous tubules

A 
not homogenous
differnt types of cells
complex stratified epithelium 
sertoli cells have sperm embedded in them 
both mitosis and meiosis occurs
71
Q

maturation of spermatogonia

A

spermatogonia –> spermatocytes –> spermatids –> spermatozoa

72
Q

sertoli cells

A

columnar epithelial cells
provide structural organisation
connected by tight junctions - BLOOD TESTIS BARRIER

73
Q

sertoli cell blood testis barrier

A

interstitial and basal compartments are separated by a cellular basement membrane
protects the sperm from damage from any toxins in the blood
spermatogonium is in close contact to eh peritubular region and blood. however just above that is the tight junctions which are protecting the more mature cels closer to the lumen. also protectin the sperm cells themselves because if they were to get into the blood they would produce antigens against the mature sperm which would have consequences for the fertilty of the male

74
Q

sertoli functions

A

supportive -nursing’
exocrine- fluid production to move immobile sperm out of testis towards the epididymis
endocrine- androgen binding protein procution, androgen receptor and FSh receptor ecpression
aromatisation of testosterone to estradial

75
Q

spermatogensis vs spermiogenesis

A

spermatogenesis:
1. mitotic proliferation
2. meiotic division - diversity
3. cytodifferentiation (SPERMIOGENESIS), package of the chromosomes for effective delivery to the oocyte round cells change to elongated sperm- packaged in a way for effective delivery. acrosome reaction

76
Q

spermatozoan structure

A

head- condensed nucleus, acrosome
midpiece- mitochondria, provide energy for ATp
tail- fibrous sheath

77
Q

organisation of spermatogenesis

A

temporally and spatially
rounds are initiated at time interveals that are constant and characteristics for each species
4 successive waves occur at the same time
human cycle = 16 days apart
adjacent segments of tubule are ither advanced to just behind

78
Q

steroid production in the testis

A

NO POSITIzVE FEEDBACK
LH and FSH from ant pituitary
- LH acts on Leydig cell –> androgens
- FSH acts on the sertoli cell –> androgen binding protein, spermatogenesis

79
Q

castrate male

A

removal of the testis- LH levels are higher than intact because there is no negative feedback from leydig and sertoli cells

80
Q

estrogen in males

A

increase with age
negative feedback to the hypothalamus and pituitary
synthesied in leydig cells, sertoli cells, germ cells and sperm

81
Q

activin male

A

androgen synthesis enhancing LH action in testis

enhanced spermatogenesis and is elevated int he epididymis and vas deferens

82
Q

follistatin in male

A

inhibits activin activity

increases progressively from the testis to distal vas deferens

83
Q

inhibin male

A

highly expressed in epidiymis and testis and regulates spermatogensis
secreted in sertoli cells
androgens stimualte inhibin production

84
Q

spermatogenesis is dependent on endocrine support

A

surgical removal of pituitary = testicular shrinkage, declinei n sperm output, arrest in spermatogenesis
leydig cells become involuted, testosterone output falls and testosterone dependent male genetalia hypotrophy
LH controls Leydig cells!!!

85
Q

sertoli receptors

A

androgen receptors - bind androgens and generate even more potent androgens than testosterone alone via 5alpha reductase activity
FSH stimulate expression of androgen receptors, inhibin ,activin and androgen binding protein
acts indirectly on spermatogenesis

86
Q

Leydig cells

A

convert lipids to testosterone

87
Q

steroidogenesis in the testis

A

leydig cell is the primary producer of steroids in the male
leydig cell releases testosterone, androstenedione and DHEA
these enter the sertoli cells and bind to ARs and convert to more potent DHT

88
Q

actios of testosterone

A

spermatogenesis
development of male physical and behavioural characteristics
gametogenesis
maintenance of reproductive tract and production of semen
maintains blood testis barrier
accessory gland function

89
Q

high E2 - follicluar phase

A

increase in cilia beat frequency

smooth muscle contractions

90
Q

high P4 phase

A

deciliation of cells

smooth muscle relaxation - therefore zygote is trappe at junction until the muscles relax and it moves into isthmus

91
Q

sperm maturation

A

maturation in the epididymis

- DNA stabilisation, chromatin condensation, concentration

92
Q

sperm storage

A

in vas eferneces before ejaculation in seminal fluid

93
Q

accessory glands in males

A 
seminal vesicles 
- alkaline fluid, fructose (energy)
- energy/ muscular contractions in female tract 
prostrate 
- alkaline fluid, enhances sperm motility 
antimicrobieal effects
bulbourethral glands 
- mucous secretion - lubrication
94
Q

seminal plasma

A

creation of alkaline environemnt in the vagina
coating the sperm cells with capacitation inhibitors- dont want sperm to start being degraded
activation of sperm
fluidizing ejaculate after 15-20 minutes (proteases from prostrate) so sperm can move within female tract

95
Q

corpus cavernosum

A

engorgement of erectile tissue with blood –> erection

96
Q

ejaculation

A

rhythmic contraction of vas deferens

97
Q

sperm movement and maturation in female tract

A

ejaculate deposited in vagina at cervical os
fluidises after 15-20 minutes
uterus provide nutrients, physical mucous consistency and aid capacitation
ocoyte attracts sperm
- chemoattactant via odorant receptors
- progesterone produced by cumulus cells and progesterone receptors on sperm head

98
Q

role of oviduct in sperm transport and maturation

A

formation of a holding reservoir i n the isthmus - so sperm can complete capacitation
binds ejactulated sperm to the epithelium

99
Q

seminal fluid in oviduct

A

quality of seminal fluid impacts on future health of the baby
interacts with female tract- promotes an immuno-tolerant environment so mother’s immune system doesn’t attack foreign thing

100
Q

capacitation

A

stripping of non-coalvently bound epidydiymal and seminal glycoproteins and sterols
decrease sperm plasma membrane stability and increase calcium permeability to increase cAMP
increased motility
female reproduction tract ideal for process due to proteolytic enzymes and high ionic strength
media supplemented with H2O2 assists with in vitro capcitation

101
Q

acrosme reactions

A

initiated by sperm contactin the zona pellucida
acrosome swells
acrosome contents are exocytosed, includes proteolytic enzymes
acquires potential to fuse tih oocyte plasma membrane
hyaluronidase assists sperm through cumulus matrix
cortical granulase fuse to egg palsma membrane and undergo exocytosis - prevents polyspermy

102
Q

zone pellucida glycoproteins

A

acellular glycoprotein coat
synthesised and secreted by oocyte in primary follicle
ZP3 allows specieis specific sperm-oocyte bidning
ZP3 target for immunocontraception - can induce a resposne against ZP3 agprotein in egg for pests

103
Q

fertilisation

A

binding of 1 capacitated perm to ZP2/3 induces acroseom reaction
penetrates ZP to the perivitelline space
binds to a fuses with the oolema via fertilin-intgerin adhesion; activated calcium waves
calicum induces realse of cortical granules and resumption of meiosis; formation of asymmetrically located cleavage furrow
meiotic division completed
- 2nd polar body and female pronucleus
formation of male pronucleus

104
Q

calcium spiking pattern in a fertilised oocyte

A

starts a few minutes after fusion
terminated at pronuclear stage
trigger the resumption of meiosis- oocyte activation, trigger release of cortical granules
gardeing of zona pellucida- zona reaction, prvenets polyspermy
preservation of euploidy- even nunber of chromosoems

105
Q

syngamy

A

formation of zygote
4-7 hours post fertilisation
fusion of male and female pronuclei

106
Q

contributions to zygote from male and female

A

male = centrosome, spindle formation

female- cell membanre, cytoplasm, organells, mitochondria

107
Q

preimplantation embryo

A

size of embryo does’t change but the blastomeres get smaller

108
Q

genetic activity in preimplantation embryo

A

first few cleavages rely on stored maternal mRNA and proteins
at 4- cell stage = wave of maternal mRNA degradation that destroys much of maternally inherited mRNA
improinting of DNA and or chromatin proteins such as histones
epigenetic process of inhertinace

109
Q

energy metabolism in preimplantaiton embryos

A

cleavage stage = pyruvate –> lactate for energy

compactino stage = glucose

Endocrinology (5 decks)

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