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1
Q

what does a steroid recpetor complex bind to on DNA?

A

SRE

or promoter

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2
Q

what cell synth steroid in the testis?

A

leydig

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3
Q

What is the process of T synth in the testis

A

LH bind LHR on leydig
stimulates the production of T from cholesterol
T diffuse into blood
Sertolic cells have FSHR
FSH bind FSHR stimulate the conversion of T into DNT by 5a reductase

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4
Q

what is the phenotype of an ARKO mouse

A

testis size 20% of normal
spermatigoenesis arrests at spermatocyte stage
female appearance

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5
Q

how is estradiol made by testis?

A

androstendione into esterone by aromatase
esterone into 17b estradiol (reversible
androstendione also into T then aromatise

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6
Q

is oestogen imp in testis?

A

yes ko mice spermatogenesis starts but fails

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7
Q

what occurs in the epididymis?

A

sperm maturation

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8
Q

what occurs in the seminiferous tubules?

A

sperm production

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9
Q

what is the purpose of the menstrual cycle?

A

release of gamete

prepare endometrium for implantation

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10
Q

what are the four phases of menstrual sycle in the uterus

A 
menstrual = failure of imp in last cycle (d1-5)
proliferative = repair lining (d5-14)
ovulation = release of oocyte (d14)
secretory = endo secrete to support implant (d14-28)
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11
Q

What are the two phases of the menstrual cycle in the ovary?

A 
follicular = follicle dev/ovul occurs at end (d1-14
luteal = corpus luteum releases prog (d14-28)
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12
Q

what is an oestrus cycle?

A

behaviour strategy to ensure mate at ovulation

inc atractiness/recpetiveness/proceptivity

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13
Q

do humans have an oestrus cycle?

A

attractivness = male prefeer female smell at ovul
receptivity - no ev
proceptivity = dance changes/female tolerate male sweat more near ovul/women isntigate sex more second half of cycle

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14
Q

describe the hormone/brain synthesis

A

kisspeptin stimulates hypothalmus to produce GnRH
GnrH stimulates the anterior pituitary to relase GN (lh and FSH
these diffuse in blood to gonads
at the ovaries Gn involved in oocyte release and sex steroid synthesis
sex steroid feedback to brain (neg and pos) and also accesory reproductive organs

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15
Q

what is puberty?

A

individual acquires the beahvioural and physiological attributes to reproduce

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16
Q

what factors infleunce timing of puberty?

A

genetics is largest factor
stressful events
intra family relationships
endocrine disruption

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17
Q

what evidence is there nutrition afffects initiation of puberty?

A 
japan 1940-70 14-12.5
spanish civil war menarche incr
cameroon rural 14.3, urban 13.2
malnutrition/athletes
pot critical weigh needed
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18
Q

what evidence is there leptin is important?

A

increases at start of puberty
KO mice = underdev gonads/ low Gn
treatment reverse abnormalities

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19
Q

what evidence that leptin not the sole signal?

A

no Leptin receptor on GnRH neurones

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20
Q

what evidence is there Kisspeptin important in puberty?

A

disrupt the kiss1 gene = infertile
treat rats with Kp = advance time of puberty
is produced in the ARc and AVPV in hypo
its recpetor increases in AVPV at puberty
recpetor expr in GnRH neurone = act GnRH

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21
Q

how does the GPR54 neurone influence transcription

A 
confirmational change 
reveals a domain
Gaq activates Phospholipase C 
Gas activates adenylate cyclase
PLC pathway activates diaglycerol Protein kinase c  cascade that activates GnRH transcription
plc pathway also release Ca
plc also act MAPK
mut in rec = delay
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22
Q

what is the link of Kisspeptin and leptin

A

leptin R on kiss1 neurone

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23
Q

what is the strucute of fsh/lh?

A

dimeric pr
ab units
b units specific

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24
Q

what are the two isoforms of lh/fsh and why do they form

A

acidic and basic

post transciriptional mod due to conditions

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25
Q

what is the properties of basic and acidic Gn

A

acididc =decrease rec bind/bioactivity and incr half life

basic = incr rec bind/bioactivity and decr half life

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26
Q

when are the differnent isoforms if the Gn imp?

A

basic FSH = select follicle
acidic FSH= follicle dev
basic LHM = young women
acidic LH= menopausal

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27
Q

what are the differences between LH and FSH release

A

FSH consitiutive pathway = little storage

LH packaged in electron dense granules in association with the storage pr secretogranin II at the mbm

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28
Q

what is the recpetor chnages thta cause LH and FSH secretion?

A

in a pit GnRH bind
conf change
Gaq reveal
a disassocaites activates PLC activates PKC and Ca
PKC act MAPK
MAPK in the nucleus effect the transcription of the subunits of gn

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29
Q

what are the regulatory drivers of folliculare dev

A

lh
fsh
follicle (oocyte and somatice cells)

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30
Q

why are the somatic cells of the follicle important

A

as the oocyte has no FSH and LH receptors

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31
Q

desccribe the development of teh primordial follicle

A 
migrate germ cell to feltal ovary
mitosis and incomplete cytokinesis (=germ cell nests)
some meiosis but arrest P1
break down cellular bridges
and flat layer of granulosa cells
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32
Q

What regulates the devlopment of the primordial follicle

A

theoocyte

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33
Q

what evidence is there that primordial germ cells in adult life in humans

A

oogonal stem cells in mice
inddx4 only exrp in germ cells detect with antibody then isol
put into mic with GFP
found GFP + cells throughout the tissue
= mitotically active germ cells that can be programmed in vivo

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34
Q

describe a primary follicle

A

oocyte still in p1
cuboidal granulosa cells
zona pellucia formed

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35
Q

describe a secondary follicle

A 
oocyte still in p1
multiple layer g.cells
zona pellucida
theca cells interna (nect to g cell imp in sex steroid synth/externa (structural support)
bigger strucuture
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36
Q

what are the singal involved in the change primary to secondary follicle and when does this chnage occur

A

GN independent
regulated by factors folicles release
OSF = TGFb (GDP and BMP15/ activins and inhibins promote fol dev) ko =infert
activins increase g.cell and stop thecal cell androgen synth
g.cell release anti mullerin hormone and kit ligand
kit ligand ko = no further dev (balance act vs inh factors )
occurs all the time/ takes 2-3 months

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37
Q

describe a tertiary foolicle

A 
oocyte
sona pellucida
theca (e/i)
g .cells = mural (wall of cavity) and cumulus(by oocyte
antral cavity (fluid from g.cell
sex steroid synth
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38
Q

singal involved chnage seconddary to tertiary follicle and when does it occur

A

FSH

every month one foolicle sel for further dev

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39
Q

hormone / steroid changes in early folliclular phase

A

no sex steroid prod = low oest = FSH rel inc
this promotes 2-3 foll change
3 foll rel sex steroids

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40
Q

what cell of 3 follicle involved in sex steroid synthesis

A

g.cell and thecal
lh bind thecal = produce androgen
androgen diffuse into g.cell
aromatase in g.cells = oest

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41
Q

hormonal changes in mid follicular phas

A

increase oest = neg feedback
decrease in FSH
sel of follicle = sensitive to FSH

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42
Q

what cell of the follicle have receptors for GN and how do these regulate steroid ynthesis

A

g.cell and theca
GPCR
Gas activate adenylate cyclase = CAMP = PKA act +phosphy pr imp for enz in steroidgenesis

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43
Q

what are the three main roles of follilce in regualting its own dev

A 
OSF = influence cumulus cells (bind ser/thr kinase - act Smad mol - translocate nuc and act as TF) = regulate g.cell prolif/diff/ estrdiol prod and metabolism
nutrients = g.cell prid chol (oocyte can't
meotic arrest (cGMP hgih - high CAMP = act Wee1, WEe1 inh MPF
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44
Q

how do oocyte and somatic cell communicate>

A

via gap junctions

connexin 43

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45
Q

whatare the layers in the endometrium and cells

A 
functional zone (lumenal and glandular epithelium)
basal zone
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46
Q

what underlies endometrium

A

myometrium

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47
Q

what layer of endometrium is shed at menses

A

functional zone

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48
Q

what change to endometrium occur during the proliferative phase of the uterus>

A 
F.zone luminal and glandular epithelium proliferation
stromal cell proliferation
endothelial proliferation (incr b suply)
glands enlarge in f zone(imp for impl)
incr cervical mucus
incr Prec expr
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49
Q

what are the changes in endometrium occur during the proliferative phase of the uterus dependent on?

A

oestrogen from developing foollicle in ovary

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50
Q

what inh classical ER rec

A

prog

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51
Q

where are classical ER rec expressed

A

epithelial and stromal cells

not static follows oest levels

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52
Q

what form of ER imp in proliferative phase

A

alpha

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53
Q

are both stromal and epithelial ER classical recptors important in proliferative phase

A

only stromal
(Balb/c mice wiht no ERa on epithelial cells and ERKO, mix so WT and KO of ERs and ERe cells)
no rec in ep sim to wt no rec in s no prolif

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54
Q

how do ERa stromal and epithelial cells communicate>

A 
paracrien signals
IGF-1 made in s cell and rec in ep
invitro stim prolif 
incr at prolif phase
oest stim IGF and IGFr 
act PKB pathway
KO = epitheial cell of endo no resp to oest
ko rec = inh oest stim proli of epithelial cells
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55
Q

are mbn bound er imp in the prolifertive phase?

A

moer mice (only mbn bound)
cant get preg/ no ovul/oestrus
comaprable to ERa KO
not sufficient

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56
Q

are GPCR ER imp in proliferative phase >

A

Ko still fertlie with norm repr histology but expr follows oest dependent manner

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57
Q

what is the role of ERa epithelial cells

A

protect against apoptosis
ko assoc with incr apoptosis
also needed with ERa stromal for secretory pr production
also imp in prevention of phospy of stromal era
= regulatory control?

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58
Q

how do OSF influence the selcetion of the dominatnt follicle

A

regulate prolif of granulos proliferation
matrix proliferation = imp for movement of follicle ot ovul
influence pest prod = incr chance of sel
incr osf in culture shown to incr quality

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59
Q

what factors infleunce the sensitivity of the oocyte to FSH levels?

A

activin / inhibin
estradiol
igfs

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60
Q

what are activin and inhibin

A

TGFb fmaily pr
dimeric
produced by granulosa

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61
Q

the role of activin

A

in arly follicle
enh granlosa prolif = incr ize inc oest =autocrine
stim FSh prod
incr FSH sens (incr rec on granulosa)

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62
Q

the role of inhibin

A

later stage of maturing ollicle
inh fsh prod
sensitise follicle to fsh (incr rec on g cells)
promote LH stim androgen prod ( in thecal cells method to inc oest feedback to decr fsh

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63
Q

how does estradiol infuelnce senstiivity of ooctye to FSH

A

enh armonatase = incr oest
stimulat g.cells LH rec
suppres FSH in apit = v lov levels

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64
Q

how do insulin like growth factors infleunce the sensitivity of oocyte to FSH?

A

stimulate g.cell prolif = more oest 7augment stim effect on gn on steroidengenesis to incr oest
(incr oest in folllicular fluid of dom follicle )

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65
Q

how is igf activated

A

norm bound bp
these inh ingf activity and in mares follicular dev
fsh stimulates prod of igfbpproteases
supr of igfbp

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66
Q

what characteritics of dominatn follicle

A

high inhibin:activin
sens to low FSH
high igf;igfbp
expr LH rec

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67
Q

describe the hormonal events at lh surge

A

lot of oest
oest threshold changes to positive feedback to hypo
ERa on kiss1 neurone in avpv essential for this
fast pulse GnRH = LH

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68
Q

what occurs in the ovary at the LH surge?

A

Resumpition of meiosis
progesterone secretion
plasminogen and prostglandins activated
corpus luteum left behind in folllicle = rel prog

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69
Q

how does meiosis resume at ovulation

A

Lh surge induce PKA and PKC pathways to produce EGF-like factors
act MAPK
this interupts cell comm by phisphy connexins43
gap junction closure
dec cAMP in oocyte
no act Wee1 = no inh of MPF - resume then arrests M2

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70
Q

describe meiosis of the released folllicle

A

asym
m1 = polarise secondary oocyte and small polar body (0.5chr no cplasm)
m2 = 2nd polar body

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71
Q

What controls the asym division of the ovulated folicle

A

position of the spindle/cortical graules/microvill reorg /myosins GTPases
important for maintenance of cplasmic stores for oocyte and sperm bind (microvilli all around oocyte - factor in ageing)

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72
Q

What changes are occuring at the early secretory phase in the uterus?

A

oest higher than start of cycle - lh still but falling
(osetrogen has primed endo with Prec)
prog produced act by Prec - inh ep prolif (stormal PR only)
stimulates decidulisation of endo
mucus thickening

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73
Q

what is decidulisation?

A

gland devleopment and secretion
stromal oedema
maturation of spiral artieries
in preperation for preg

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74
Q

what hormonal chnages occur at the late luteal phase?

A

decrease in prog as corpus luteum degen

decr oest feedback to a pit decr lh

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75
Q

what hormonalc hanges initiates menstruation?

A

withdrawl of prog from endo

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76
Q

what physiological chnage sin menstruation?

A

shedding of fucntional layer is progressive process
some areas unshed/partial/completly to decrease risk of haemorrage and infection
pre men = extensive b,vessels/tall columnar ep cells/tooth glands
early zonal shedding= linear cracks/detached ep/glands stumps and surface ep
later zonal shedding = multiple tubes and remenants of glands an d b vessels
healing = fibrin matrix and new ep cells/ new and unrepaired epithelium/ small and cuboidal ep cells

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77
Q

what vascular chnages ccur in menstruation?

A

spiral artires constrict
and vaso dilation
pot mediated nitric oxide prostoglandins?

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78
Q

what causes matrix degradation during menstruation?

A

stroma expresses MMP1/2/3
epithelium expresses MMP7
regulated by progesterone

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79
Q

what hormone rescues the corpus luteum at preganancy?

A

human chorionic gonadotrpohin out of the ST from the embryo

signals via LH rec

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80
Q

what is the corpus luteum?

A

after ovulation what is left behind of the follicle
thecal cells beocme small lutein cell that prod prog
granulosa cells (mural) form large lutein cells that prof prog and oestrogen
LH req for maintenace

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81
Q

what is ovulation?

A

release of the secondary oocyte from follicle

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82
Q

what cells stay asssociated with the oocyte after ovulation

A

cumulus cells

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83
Q

what is the epididymis

A

sperm collection and maturation (here 14 days)

beocme motile

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84
Q

what is the vas deferens

A

transport tube in testis = sperm forced here by contraction in sexual arousal

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85
Q

what are the accessory glands

A

ampulla and seminal vesicle (reservoir end of vas def)
ejaculatory duct
prostate gland (prostate fluid imp in semen)
bulbourethal gland adds fluid at ejac

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86
Q

where does sperm production occur?

A

seminiferous tubules

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87
Q

what are the two main cell pops of the seminiferous tubules

A

sells of spermatogenic lineage

sertoli cells

88
Q

where do you find spermatoagonia

A

near the basal comparment of sertoli cells near myoid cells and capillaries

89
Q

where does spermatogenesis occur

A

sertoli cells
start at basal lamin
move towards adluminal compartment more developed sperm

90
Q

1 germ cell undergoes how many round of mitosis to become spermatagonia

A

4
produes 16 cells
all 2n

91
Q

what occurs to make spermatagonia a primary spermatocyte?

A

growth

92
Q

what occurs to go from primary to secondary spermatocyte

A

one round meiosis

93
Q

secondary spermatocyte to early spermatid

A

another round meiosis

94
Q

late spermatids different from early spermatids

A

have flagella but cytoplam still joined

95
Q

how many rounds meiosis and mitosis in spermatogeneis

A

4 mit

2 meiosis

96
Q

how many sperm cells produced from one germ cell

A

64

97
Q

what is the final stage of spermatogensis

A

spermiogensis
maturation early spermatid to spermatazoa
cytpolasmic remodelling to get classic sperm shape

98
Q

the process of spermatid remodelling in spermiogensis

A

distal centriole = flaellum dev from MT of centriole
proximal imp for dev of sperm head
loss of resiudal body4
mitochondria
Acrosome formation - a golgi body derived vesicle whcih forms a cap

99
Q

what enzyme in the acrosome cap?

A

hyalouronidase = released when sperm reach oocyte

digets the cumulus cells and zp

100
Q

3 main parts of sperm strucutre

A

head
mid piece
prinicipla piece

101
Q

what features in the sperm head?

A

DNA heterochromatin
perinuclear space
cell mbn
acrosome soread over the nuclear apex, DRY192 gene encodes a pr that anchors nuc mbn to acrosome cap
neck contains mito sheah around mt network

102
Q

what features in the sperm mid piece

A

mito sheath
with helicoidally arranged mito
dynein needs ATP
sep from prinicipla piece by jensens ring - dense material

103
Q

what features of the principal piece?

A

fibrous sheath
9x2 mt
no mito

104
Q

where do sperm become motile?

A

in epididymis aar of DHT

105
Q

what is spermiation?

A

the release of spermatids from sertoli cells prior to passage in epididymis
occurs over days
more streamlined sperm produced

106
Q

how many sperm start developing each day and how many complete?

A

3x10*6
half die
but waries lot person to persom
even between people = one study 3 years 20-170mil/ml

107
Q

how many sperm per ejaculate

A

39x10*6 less that 40% motile less than 4% norm morphology

108
Q

what is the current trend for sperm count and why

A

decrease
age/smoking/oxidative stress
decr 59.3%
below 20 mil /ml big effect of fert suc above no big diff

109
Q

how many sperm in the female tract

A

vag 107
uterus 105
10*2 f.ube ampulla

110
Q

what changes to the cervical mucus occur at ovulation

A

prog dom
decr mucin produced
loss hydration
prevent sperm entry

111
Q

what some of the sperm defects seen in inferile males

A

globosoospermia - round head sperm/no acr cap/ mut in DRY 192 = cant fert

112
Q

what factors influence male infertility

A

hormone imbalance
infection
morphology
problem with ejeaculation

113
Q

what probelm arise from ICSI

A

bypass a natual selection point = no selection on good fertility genes
in mice = ageing and tumour incr and decr in offspring

114
Q

what occurs as soon as sperm is deposited in the vagina an dwhy is this important?

A

forms fibrin like gel

which retians sperm and biffers against acidic cervical fluid

115
Q

what is the function of human cervical mucus

A

protect cervix from hostil vaginal env
resticit sperm entry to the peri ovulatory period when the mucus is less viscous
restrict abnormal sperm entry
E ?
remove factors from sperm eg chol and anti capaacitation factors that prevent sperm occuring
(only when no Prog sperm can penetrate)

116
Q

where does fertilisation occur?

A

at the ampulla of the fallopian tube 10*2 reach 2cm distance

117
Q

how do sperm get to the fertilisation area?

A

own motility
uterine cillia dev a current?
but immotile isthmus of oviduct

118
Q

what is capacitation?

A

acquire fertilisation competence

119
Q

why is capacitation necessary?

A

alllow sperm to bind Zp

120
Q

what drives capacatation?

A

sterol bp initaiate loss of chol incr mbn fluidity

needs external HCO3 = adenyl cyclase promotes cAMP dep tyrosine phosphy of specific pr
incr intracell ph = act ion channel in flagella (k entry= hyperpol=ca influx by catsper)

ion inlfux =motility change

121
Q

what changes occur to sperm at capacitation?

A 
hyperactivee motility
detach from oviductal epi
removal of seminal glycopr 
entry ca and rel from internal stores
export proton
cytoskel change
expose rec for zp2 3
122
Q

prior to fet what oocyte surrounded by

A

cumulus oophurus

123
Q

what are the six stages of fert

A 
zp bind
acrosome reaction
penetrate zp
bind p mbn
fusion 
nuc enter cplasm
124
Q

what rec is necessary for zp binding

A

zp3

125
Q

what are the two steps zp binding

A

= intial b1-4 GALT independent
SED1 sperm rec imp
firm sperm zp binding and induce aggregation of sperm rec GALT

=GALT dependent
binds ZP3
binding - cluster of rec on side of sperm head,
acrosome rel acrosin - digest whole through zp
zp2 imp for skeeping sperm and sp attach
in humans zp1-4 imp

126
Q

what is the zona pellucida

A

glyco pr coat layer inc pr zp1-4 human

1-3 mice

127
Q

what triggers acrosome reaction

A

GALT sperm rec bind ZP3

but observed in mice areaction before zp = no galt

128
Q

what changes occur at acrosome reaction

A

p.mbn of spern and outer acrosom mbn multiple fusion

anterior sperm head enclosed by inner acrosomal mbn

129
Q

what is acrosome reaction dependent on?

A

Ca
plc act ca influc
induce exocytosis of cap
and convert proacrosin to acrosin

130
Q

how do sperm penetrate the zp

A

motility

proteases and glycosidase

131
Q

where does the sperm binding to the p.mbn occur

A

at microvilli free region far from meta chr

132
Q

how does sperm binding to the p.mbn occur?

A

by equatorial segment
(same pr that drive fusion?)
pot vitronectin rel at acrosome bidge helps other bind?

133
Q

what pr are important for the fusion of the sperm and egg

A

CD9=
on ooocyte mbn in microvilli
KO no fusion

izumo = immunoglobin fam pr KO bind not fuse

134
Q

what happens to the sperm tail at entry?

A

into egg

sperm bring centriole - form aster for first mitotic div

135
Q

What activates the egg

A

series of intracellular calcium oscillatiion
ER rel 40-400nm Ca
occur one min after fert
one min duration and between 3-15 mins
need internal ca and doesnt occur in ca free external media

136
Q

what how long do calcium oscillations continue for

A

pronuclear fromation

137
Q

why calcium oscillation importnant?

A

cortical granule extension
resumption meiosis
pronuclear formation

138
Q

how is polyspermy prevented

A

ca dependent fusion and exocytosis of cortical granules w enzymes at mbn
these inc protease which cleave ZP2
enz also induce crosslink of zp = no bind/entry
also strip sperm rec from mbn. and harden zona by peroxidase mediated oxidation

139
Q

what occurs in the prelacunar phase?

A

trophoblast differnenitiates into two pops

140
Q

what are the two populations of trophoblast cells at the prelacunar stage

A

cytotrophoblast = mono nuc/nearer embryonic disc/stem cells prlif and fuse
synctitrophoblast - syncital fusion of CT forms multinucleated ST/sgl cell continuous layer /terminally differentiated/inasive ptype/in contact w mat cells/expands and surrounds blastocyst

141
Q

when does the lacunar phase occur?

A

8 days pc

142
Q

what occurs at the lacunar stage

A

vacules appear in ST and coalescce= lacunae
llacunae sep by bits ST called trabaculae
blastocyst embedded

143
Q

when the lacunar sytem has developed what layers of placecnta can be categorised

A

chorionic plate
lacunar system
trophoblastic shell- contacts endo and anchors

144
Q

how does maternal blood enter the lacunar sytstem

A

ST pentrate interstitium of endo
contact mat capillaries and venous sytem of endo
erode vessels
=mat blood enters

145
Q

how do primary villous trees form and when?

A

CT from priamry choironic plate invade downthrough the trabeculae down to the trophoblastic shell and contacts the lacunae.
d12-15 pc

146
Q

how and when do secondary villous trees form?

A

mesenchymal cells penetrate the primary villous between days 15-21

147
Q

when and how do tertiary villous trees form?

A

when the b vessels start to form from mesenchyme cells derived from hemangioblastic progenitor cells
vasularisation of the strucutre and occurs days 18-20

148
Q

when and how does connection of maternal and fetal circulation occur

A

-5 weeks pc
fusion of the allantois with the choironic plate form = umbilical cord forms
choironic plate fuses with the villous cap

149
Q

what are the four main step of villi development that continue though pregnancy

A

CT prolif
CT fuse
mesenchyme migr
formation of vascularised stromal core

150
Q

what featres are there fo theird trimester villi?

A

stem villi

terminal villi = specialised fr transport

151
Q

what ST specialised for

A

nutrient and gas exchange

152
Q

what changes in morphology happen to placenta in 3rd trim to support dev fetus

A

decr diameter of villi
thinning ST
highly vascularised
vasculosynctial mbns = capillaries v close to ST

153
Q

what the function of the placenta

A

nutrient gas exchange
hormone synth
protective barrier

154
Q

what cells of placenta make hormones

A

ST

hcg and prog estradiol

155
Q

role of the hormones prod by the placenta

A

hcg= save cl and essential for norm preg
prog=inh myometrial contraction/ strengthen connective tissue
oest= stim growth of brest tissue and myom layer/incr uterine b.flow

156
Q

hwat metabolic adpatation occur in preg

A

1st trm = facilitate fat storage

3rd trim= mobilisation of fat stores by placental lactogen/gf make insulin res

157
Q

how does the placenta act as a protective barrier?

A

cell surface transporters MDR! and BCRP , pump toxins out of placenta

158
Q

why is there no immune reaction in pregnancy?

A

fetus allogenic
st dont have MHC class 1 antigen = hide
represed mat immune syst

159
Q

what are hofbauer cells

A

fetla macrophages
derived from mesenchymal stem cells
promotes placenta angiogenesis

160
Q

what change occurs to blood flow and how?

A

35-50% incr out put

by incr CO/sv/hr/ decr res

161
Q

what changes in flow occur in the first 20 and last 20 weeks ?

A

incr in flow aar of incr flow ratte

incr in flow aar of incr diameter of UA

162
Q

what stimulates the vascular chnages in preg?

A

metabolic
mechanical
hormonal

163
Q

what signals do the endothelial cells of vessels release

A

prostaglycin
NO (oest effects, in primates incr oest incr no =dil)
EDHf

164
Q

in the first 11 weeks what why is there no blood to placenta

A

extravillous trophoblast cells that invade the maternal spiral arterioles and accumulate to form plugs
also line and remodel the maternal SA to allow the blood to get to intervillous space and not dmaage

165
Q

what are the two type of CT

A 
extravillous trophoblast (imp in plugs)
villous trophoblast (proliferate and fuse = the stem cells)
166
Q

where are the two locations EVT invade

A

spiral arteries and uterine glands

167
Q

aside from damage why trophoblast plugs important

A

hpoxic condtions in placenta imortant for DNA transcription

168
Q

how and when do trophoblast plugs form

A

invade from implantation
but CT radiate away from shell to group of glands
these cells form the plugs of the SA (EVT)

169
Q

what two components remodel the artieries

A

maternal leukocytes *unk and macrophages)

trophoblast

170
Q

the steps of remodelling

A 
1-leukocyte - vsmc interactio
2-leukocyte- ecm interaction
3-trophoblast - vsmc interaction
4-trophoblast - ecm interaction
l
171
Q

consequence of remodelling

A

loss of vsmc =insensitive to maternal constriction
loss of elastic lamina - loss of ealstic recoil and irreversible expansion of the arterial channel.
low res blood to intervillous space

172
Q

when does remodelling occur

A

pre 11 weeks to 18 weeks

173
Q

where does the trophoblast invasion continue until

A

reaches arterial segment sin the inner thrid of hte myometrium

174
Q

difference in the remodelling in the myometrium

A

less lukocytes
mainly trophoblast
mosty in 2nd trim as takes times to get past functional zone

175
Q

what happens do plugs after 11 weeks

A

displaced and intervillous space a shut oxygenated blood passes through at low pressure

176
Q

% of coneptions reach= implantation]
recognised preg
live brith

A

75
60
50

177
Q

effect of age on success getting preganat

A

decr due to oocyte quality

incr risk misarriage down

178
Q

how successful is ivf

A

29% clinical preg

21% live birth

179
Q

how common are chr abnomalites in oocyte/blastocyst/zygote

A

20
50
40

180
Q

first trimester and chr abn

A

90% chr abn misscarry 1st trim

60% of all 1st trim miscarry chr abn

181
Q

why is it difficult to determine embryo chr

A

genetic mosaicism

182
Q

diff ways detect chr abn

A

fish
TE biopsy
comparative genomic hybridisation

183
Q

other factors link to miscarriage

A

lif imp
poor decidulistion
SA not remodel
immune recog

184
Q

what is pre eclampsia

A

complex heterogenous syndrome

185
Q

what symptoms of pe

A

in 3rd trim hypertension/oedema/proteinerea someimtes fgr

186
Q

what are risk factors of pe

A

hyper tension 20%
prev pe 23%
chronic renal disease 30%
diabetes

187
Q

how to treat pe?

A

early delivery

188
Q

is pe big porblem

A

yes 50000=70000 each yr die worldwide

189
Q

causes and physiological links of pe

A

problems with placenta
remodelling failure -no incr b flow stll high pressure
severe early onset - fail to remodel in myometrial seg
result in shear stress in intervillous space = oxiddative stress?
release of microparticles = immune/vascular act result in decr atp
and decr uteroplacental perfusion
activation of endo cells = pedema/proteinurea/platelet act

190
Q

how could transriptomics be used to treat PE

A

look at mrna levels
see if common gene inv
give idea of the molecular pathways inv

191
Q

long term effect of pe

A

incr risk nearly by 2 of cardiovasc disease

incr pe risk again

192
Q

how common is fgr

A

5-8% preg

75% missed antenatal

193
Q

the consequence of fgr

A

iatrogenic preterm brith
neonatal morbidity
lifelong disabilities
stillbirth (more than 50% sill birthfgr)

194
Q

what causes of fgr

A

placental dysfunction

placentla abnoramlities

195
Q

what are the placental abnormalities that can cause fgr and how do they

A

abn dev

  • decr villous tree/dec SA
  • thicker ST
  • cell turnover/less CT prolif and ST growth = less branched smaller placenta with limiting supply to fetus

Abn blood supply

  • no remodel=decr supply
  • no blood flow in diastole shwon by doppler
  • decr mat perfusion
  • werid cord placement
  • plac arteries constrict

REduced Activity nutrient transporters

  • syst A decr 50%
  • ca x2 in st of fgr

Endocrine function
-lower conc of placentlal hormones in mat blood
hpl/pgh/pigf

196
Q

how are placental probs currently detectted?

A

ultrasound/doppler utlrasound

197
Q

future prospects of monitoring for fgr

A

placental ultrasound

measure conc of placental hormones in mat cric

198
Q

similarities between human and mouse placenta

A

hemochorial - T cells bathed in mat blood
have decidua/evtchoironic plate and u cord
transport syst - glut1
dim diffusion characteristics

199
Q

how is mouse differnet to human placenta

A

labyrinthe - T lined mat blood spaces interwoven w fetal capillaries in a labyrinthe
2 zones - spongiotrophoblast(for endocrien and labyrinthe
hemotrichorial - 3 layer t cekksbetween mat and fetal blood
have two types invasie T=giant cells and endovascular T

200
Q

what is the effect of IGF 1 ko

IGF 2 ko

A

fgr

fgr and placental growth restr

201
Q

ko igf2 in plac only via mut in prmoter

A

fgr and placenta growth rest= show reduced plac size a cause of fgr

202
Q

ptype of no igf2 in placenta

A

decr i labyrinthe by 50%
decr spongiotrophoblast zone
thicker exchange barrier

203
Q

effecton transport system of igf2ko

igf2 plac only

A

decr syst a at d19

no decr elevated at d16 (perhaps upreg to compensate for decr growth

204
Q

when are Gc administered therapeutic

A

labour at les than 32 weeks to get lung dev

205
Q

whats the role of 11b hsd2?

and role in fgr

A

converts cotrisol to cortisone
expr in st
decr in fgr

206
Q

impact of gc on placenta dev

A

gc to preg rat = decr fetal and placental weight /decr syst a
ko 11bhsd2= model fgr supports expsure to cotrisol casue fgr

207
Q

impact of gc on human cells

A

impairs angiogensis
decr igf1 expr
incr vasocon of arteris

208
Q

what is the barker hypothesis

A

low weight at birth less than 5.5lb = increase risk of disease later in life
inc t2 diabetes every incr of 1kg in bw decr risk by 25%
obesity = both low and high weight maker more liekly (43/34)

209
Q

studies shown the impact of stress and undernutrtion

A

sheep - pr rest 60 days b4 preg and 30 days after = preterm delivery and neonatal death
humans - dutch hunger winter, low mat bmi famine b4 or in early preg had early delivery

210
Q

impact of stress at preimplantation

A

mice fed low pr diet at preimp
= blastocyst reduce cell no
both = acc postnantal growth /hypertension
female offspring- decr b weight
male offspring - incr systolic bp, abn org;mass ratio

211
Q

do culture condtions effect mouse embryos?

A

yes decr in no of TE cells in ivf

decr in icm due to embryo culture

212
Q

what genes effected by culture conditioNS

A

imprinting

213
Q

example of an imprinted gene effcet by cuturie

A

h19 biallelic after culture

negative reg of igf2 - decr in igf2 expr

214
Q

long term effects of culture onbehaviour in mice

A

elevated pllus maze test showed less anxiety and memory

215
Q

effect of stress in preganancy

A

decr fetal growth
rats synthetic gd decr placental growth and bw
rats undernutrtion decr 11bhsd2

216
Q

what is glycyrrhiz contain?

A

11b hsd2 inh

more than 500mg/week= earlier labour/cognitionve beahv diff/incr contrisol effecting brain dev

217
Q

pot treatments of stress

A

omega 3 = blocks high bp

leptin - rescues mismatich ptype reset E homeostasis pathway

Human Reproductive (1 decks)

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