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Endocrinology > 2. Conception and Pregnancy > Flashcards

2. Conception and Pregnancy Flashcards

Sexual differentiation + Pregnancy and partuition

1
Q

conception vs fertilization

A

CONCEPTION = not a scientific terminology, the idea that life is coming
*conceptio = to learn,
FERTILIZATION = physiological process by which male and female pronuclei come together to form a new set of chromosome

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2
Q

how does the sperm enter the egg at fertilization?
5 steps ish

A
  1. sperm has ZP (zona protein) binding receptors (which are glycoproteins). Zone proteins on the zona pellucida recognize the ZP receptors at tip of sperm’s head
  2. sperm comes near egg –> produces enzymes = acrosomal reaction –> breaks down zona pellucida –> gains entry
  3. sperm cell membrane merges with cell membrane of oocyte
  4. entry of sperm into oocyte triggers cortical reaction = release of Ca2+ from granules –> solidifies zona pellucida to prevent other sperm from coming (polyspermy)
  5. once male pronuclei enters, then second meiosis of oocyte happens
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3
Q
  • what are germ cells?
  • are germ cells gonadal in origin?
A
  • specialized cells that are differentiated to/destined to form either egg/oocyte or sperm
  • no! germ cells don’t differentiate within the gonad! they come from outside the future gonad
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4
Q

what are the 2 groups of cells identifiable physically after fertilization? Will become what?

A
  • inner cell mass –> becomes fetus
  • trophoblast –> becomes placenta
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5
Q

what are the 3 layers of cells during embryogenesis?
- future gonad arises from which layer? vs germ cells? –> consequence?

A

ectoderm, mesoderm and endoderm
- future gonad comes from endoderm
- germ cells come from allantoic ectoderm
- consequence: germ cells have to travel/migrate to mesoderm –> migrate to endoderm (?) and then along the hindgut to the genital ridges (future gonad)
*once they reach genital ridge, they are committed to becoming either a sperm or an oocyte

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6
Q

does germ cell differentiation depend on their sex chromosome constitution? explain

A

no! it does not! it depends on whether the genital ridge has begun to develop into an ovary or a testis (ie the chromosomal sex of the somatic cells in the genital ridge)

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7
Q
  • germ cells are polar/nonpolar during migration
  • where do they migrate from/to?
  • migration involves (2) from the leading edge and (2) from the lagging edge = _______ movement
A
  • polar!
  • migrate from ectoderm to endoderm to genital ridge
  • involves cell protrusion and adhesion to the leading edge (and the extracellular matrix) + detachment and retraction from the lagging edge/back end
    = amoeboid movement
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8
Q
  • how do germ cells know where to go during migration?
A

by somatic cells! somatic cells secrete chemoattractants or chemorepellents to create a path for primary germ cells
- primary germ cells have receptors for chemo attractants (allow for protrusion and attachment) and chemo repellents (allow for detachment and retraction)
*additional regulation of chemo attractants/repellants = sequestration or destruction of them

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9
Q

which 2 pairs of ligand/receptors direct the primary germ cell movement?
- what type of receptor?
*what happens if one of these 4 is absent?

A
  • KITL (KIT ligand) with KIT receptor (an RTK)
  • CXCL12 (ligand) and the CXCR4 receptor (GPCR)
    *if absent –> movement of primary germ cells is disrupted
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10
Q

what happens after the germ cells arrive at the genital ridge?
- 3 step process ish

A

sexual differentiation!
- chromosomal sex (XX or XY) –> gonadal sex (testes or ovary) –> phenotypic sex (external genitalia and reproductive tract)

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11
Q

X vs Y chromosome
- length?
- represents __% of genome?
- encodes how many proteins?
- genes regulate reproductive functions?

A

X chromosome:
- 160 megabses (Mb) long
- represents 5% of haploid/whole genome
- encode 850 proteins
- several of these genes regulate gametogenesis and hypothalamus-pituitary function BUT most regulate non-reproductive functions
Y chromosome:
- 60 Mb long
- represents 2% of genome
- encodes 57 proteins
- most of these genes regulate reproductive functions

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12
Q

how many chromosomes in normal male vs female?
- name of syndrome + how many chromosomes:
- XXY?
- XO?
- YO?

A
  • XY or XX –> 46
  • Klinefelter syndrome: XXY –> 47 chromosomes
  • Turner’s syndrome: XO (absence of Y) –> 45 chromosomes
  • YO = non-viable
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13
Q
  • central dogma of sexual differentiation?
  • pioneer experiment?
  • conclusion?
A
  • central dogma = female is the default and being a male is an active process
  • remove undifferentiated testes from male rabbit embryos –> found that embryos developed female reproductive tract and female genitalia VS remove undifferentiated gonads from female embryos –> developed into female features
  • TESTES are essential for male sexual differentiation, but ovaries are NOT necessary for female differentiation
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14
Q

Genital ridge
- becomes what for male vs female? ie which duct stays/degenerates? –> the duct develops into what?
- what is the name for common primordium for external genitalia? –> become which 2 for male vs female?

A

Genital ridge –> female
- Mullerian duct stays, wolffian duct degenerates
- female tract = oviduct, uterus, upper vagina
Genital ridge –> male
- Mullerian duct degenerates, wolffian duct stays
- male tract = epididymis, vas deferens, seminal vesicle
UROGENITAL SINUS!
- female: clitoris and vulva
- male: penis and scrotum

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15
Q

Men:
- mesoderm develops into _________ _______ –> has which 2 types of cells? cell type?
- function of these 2 cells?

A
  • mesoderm –> genital ridge –> sertoli cells and leydig cells –> both are somatic cells (not germ cells)
    SERTOLI –> mullerian duct regression
    LEYDIG –> wolffian duct stabilization –> leads to male external genital differentiation
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16
Q
  • which cells produce testosterone in the testes?
  • how does testosterone concentration change in early male development?
  • function of testosterone (2)
A
  • somatic cells (Sertoli and Leydig cells) in testes
  • goes up in male fetus –> comes down (testes descent) at about 20 weeks of embryonic development
  • testicular differentiation + germ cell differentiation
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17
Q

why is ultrasound sex determination done at 20 weeks of gestation?

A

because that’s when testes descent is complete

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18
Q

what are the pre-requisites for normal sex differentiation? (3)

A
  1. normal intact chromosome complement (XX or XY)
  2. chromosomes need to have fully functional sex determining genes
  3. cells in differentiating gonads have to synthesize steroid hormones (especially testosterone) –> intact steroidogenic pathway and receptors
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19
Q

how can sexual reproduction produce new combinations of genes?
- when does it happen?

A

crossing over/ recombination process! between 2 sister chromatids (1 from dad, 1 from mom)
- in meiosis

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20
Q
  • what is the problem in recombination/crossing over between sex chromosomes?
  • which parts are involved in recombination?
A
  • chromosome X and Y are not the same size! X is a lot bigger!
  • only the pseudoautosomal regions undergo recombination! (PAR regions)
    *pseudo bc only region involved in recombination
    *autosomal bc they act as autosomal (but they’re actually sex chromosomes)
  • PAR regions are at top and bottom of both X and Y chromosome
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21
Q

which part of the Y chromosome contains the SRY gene?
- function of SRY?

A
  • the male specific region of Y (MSY) (middle portion of the Y chromosome) –> specifically really close the the top PAR region of Y chromosome!
  • SRY –> gene that codes for a protein –> allows bipotential genital ridge to become a testis
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22
Q

what happens if SRY gene is transferred to X chromosome through recombination beyond PAR1?
*mouse experiment?

A

fertilization of a sperm with (X and SRY) –> produces an XX male phenotype
*injected SRY genes in a fertilized egg –> put it in mouse (= transgenic mouse) –> developed into XX mouse with testes and external male genitalia
*knew he was XX (and not XY) from karyotyping!

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23
Q

how can there be a XY female?

A
  • SRY gene was deleted OR mutant SRY gene on the Y chromosome –> resulting on non functional SRY protein
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24
Q

what is a characteristic sequence of the SRY gene?
- how can SRY proteins regulate transcription of other genes? –> SRY = what?

A
  • an 80 aa region of SRY gene shows homology within the high mobility group (HMG proteins) –> this conserved motif (HMG box) possesses DNA binding activity –> this sequence is found in many nuclear proteins that interact with DNA (either as transcription factor or transcription regulators)
  • SRY protein binds to DNA to induce transcription of other genes –> SRY = transcription factor!
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25
Q

how many mutations in SRY gene can cause XY females in which region of the SRY gene?

A

11 mutations! in the HMG box

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26
Q
  • how long is SRY gene expressed?
  • consequence?
A
  • around 2 days! from 10.5 days post coitum (dpc) to 12.5 dpc
  • consequence = ther must be another thing that drives sex determination! –> sox9! (a TF)
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27
Q
  • how is Sox9 regulated? (2)
  • sox9 stimulates expression of which other genes? (3)
A
  • first requires SRY to activate, then, it can drive its own gene expression bc it’s a TF
    1. FGF9 –> growth factor
    2. PGD2 –> prostaglandin D2 –> growth factor
    3. AMH –> anti-mullerian hormone –> represses mullerian ducts
28
Q

in the ABSENCE of SRY genes, which signaling molecules allow genital ridge to be converted to ovary?

A
  • RSPO + WNT4 + FOXL2 (TF) –> function together to “secrete” follistatin (another signaling molecule) –> necessary for female phenotype development
29
Q

male and female phenotypic development depend on which signaling molecules?

A

MALE:
- sox9 –> FGF9, AMH, PGD2
FEMALE:
- WNT4, RSPO1, FOXL2

30
Q

how does AMH signal for the regression of _________ duct?
- what type of receptor?

A
  • TGF-b receptor = serine threonine kinase receptor
  • AMH binds to AMHR2 –> recruits AMHR1 = heterodimerization –> phosphorylates itself –> phosphorylates smad 2 and smad 3 –> recruit smad 4 –> serve as TF –> enter nucleus to drive expression of pro-apoptotic genes!
  • AMH receptors are present on mullerian duct cells –> apoptosis = regression
31
Q

study hinted that Wolffian duct regression is also hormonally regulated
- which receptor? expressed where?
- ligand for receptor?
- receptor drives expression of what? through which type of receptor/pathway?
- this second receptor/pathway does what?

A
  • NR2F2 (nuclear receptor) (also called COUP-TFII) –> expressed in mesenchymal cells surrounding Wolffian ducts
  • unknown ligand
  • NR2F2 inhibits expression of FGF (growth factor) –> FGF receptors (RTK through ERK1/2 pathway) are present on Wolffian duct cells
  • FGF drives the growth of wolffian ducts!
32
Q

explain how NRF2 signals for the regression of the Wolffian duct

A
  • normal expression of NR2F2 inhibits secretion of FGF growth factor–> so no growth of Wolffian ducts = Wolffian ducts degenerate –> Mullerian duct is retained –> only development of female reproductive tract
  • VS female embryos lacking NR2F2 (knockout mice) –> FGF is expressed –> Wolffian ducts develop –> mice developed male and female reproductive tracts = intersex (= lethal)
33
Q

are both male and female reproductive tract development regulated by hormonal signals?
- active process?

A

yes! both require active process!
MALE –> SRY –> sox9 –> AMH –> mullerian duct degeneration
FEMALE –> NR2F2 –> FGF –> wolffian duct degeneration

34
Q

what is the physiological point that marks the beginning of pregnancy?

A

implantation! bc until then there is no physical connectivity btw growing embryo and uterus

35
Q
  1. where does fertilization of the ovum occur? ____A______
  2. what move the zygote along the ___A_____ to the _____B______
  3. zygote starts to divide + derives its energy from (2) until __________
A
  1. in oviduct/fallopian tubes
  2. ciliated cells (cilia of the epithelial cells)! move zygote from oviduct to uterus (but before ovulation, cilia move sperm from uterus to fallopian tube!)
  3. derives energy from oviductal and uterine secretions until implantation! (only then does the zygote has access to blood supply of the mother)
36
Q

what action is an evolutionary step that provides significant advantage to the conceptus (of mammals vs birds)

A

the attachment of the conceptus to the endometrium to form an intimate but temporary (transcient) relationship with the uterus

37
Q
  • until # cell stage, cells are _______
  • at # cell stage, cells differentiate into (2) = _____A_____
  • _____A_____ enters uterus by __-___ days after fertilization
  • implantation occurs __-___ days after fertilization
A
  • 8 cell stage –> cells are totipotent (can form embryonic or extraembryonic cell)
  • at 16 cell stage –> cells differentiate into 2 types of cells: inner cell mass and trophectoderm (forms all extraembryonic tissue and establishes contact with endometrium) –> blastocyst/trophoblast
  • blastocyst enters uterus 5-6 days
  • implantation 7-8 days after fertilization
38
Q
  • define implantation
  • implantation involves what?
A
  • implantation = embryo attaching to endometrium (embryo literally disappears into endometrium in humans)
    *special process unique to primates: deciduation/decidualization (?) –> decidual cells increase the thickness of endometrium
  • involves apposition of microvilli present on trophecoderm cells with the pinocytes (fused microvilli) on the endometrial cells
39
Q

cell differentiation, migration of blastocyst and implantation all occur under influence of rapidly rising _______ (what type of hormone?) from what?

A

progesterone! (pro gestation) steroid hormone
- from the corpus luteum in ovary

40
Q

what is the maternal recognition of pregnancy?
- contact between (2) produce which hormone? by which cells? and eventually what produces it?
- describe this hormone: type, subunit, function

A
  • when embryo starts sending signals that it’s present
  • contact btw endometrium and trophectoderm cells (ie implantation)–> embryo (trophectoderm) produces human chorionic gonadrotrophin (hCG) –> eventually placenta produces it
  • peptide hormone! 2 subunits coded by 2 different genes: alpha chain (same as FSH/LH/TSH) but different b chain
    function = promotes corpus luteum in ovary to maintain progesterone production until placenta takes over
41
Q

placental hCG gives signal to ______ _____ to continue producing __________
- why?

A

gives signal to corpeus luteum in ovary to continue producing progesterone
- bc you don’t want other follicles to continue developing if pregnancy happens

42
Q

how do pregnancy sticks work?
- antigen vs antibody?
- control?

A
  • detect presence of hCG!
  • antigen = hCG –> lower part of stick has antibody (something that recognizes hCG) and coloring agent!
  • control = a 2nd antibody against first antibody (that recognizes hCG) OR against the coloring agent –> tells you that the process of antigen-antibody works!
43
Q

changes in the uterine endometrium during the menstrual cycle:
- day __-___: __________ + beginning of what?
- days __-__: which hormone regulates which phase –> endometrium _______
- day ____: __________
- days ___-___: which hormone regulates which phase?

A
  • days 1-3: breakdown of endometrium = menses + beginning of follicular development
  • days 3-14: follicular development + estrogen (from growing follicle) regulates proliferative phase: endometrium thickens
  • day 14: ovulation
  • days 14-28: progesterone (produced by remaining follicle/corpus luteum) regulates secretory phase –> thickened endometrium acquires secretory abilities –> secretes everything necessary for embryo to survive
44
Q

which (2) sources of E are secreted for embryo survival?
- which cells synthesize ________ –> regulated by which hormone?
- source of energy necessary for embryo to do (5)

A
  • carbohydrate and glucose
  • endometrial cells synthesize glycogen –> regulated by insulin –> secrete glucose and carbs
  • initial development, proliferation, differentiation, attachment and secretion
45
Q
  • what is the shape of placenta for primates? describe
  • where should the placental disk NOT be?
A
  • discoid placenta (disk shaped placenta –> not spread throughout the entire uterine body) –> round patch of chorionic tissue that forms the fetal-maternal interface
  • should not be at the cervix! should be on the side
46
Q
  • what determines the type of placenta?
  • placenta in primates is called ___________. why?
  • how many layers? describe
A
  • the number of layers of cells involved in formation of placenta
  • hemochorial placenta: chorion/fetal side = directly exposed to blood
    1. blood vessels of fetus
    2. extracellular matrix
    3. chorionic cells
    4. maternal endometrial cells
    5. extracellular matrix
    6. maternal blood vessels
47
Q

metabolic exchange between mother and fetus:
- what is exchanged (2)
- what is NOT exchanged (2) (except 1) –> consequence?

A
  • glucose and aa are exchanged
  • lipid and protein (except IgG) are NOT exchanged –> fetus synthesizes its own lipids and proteins
48
Q

what crosses placenta, what doesn’t cross? Which hormones cross?

A

CROSSES:
- lipid soluble hormones
- toxins and substances: alcohol, lead, mercury, antibiotics, medications
- many pathogens are known to cross; HIV, herpes virus, syphillis bacteria
DOESN’T CROSS:
- peptide hormones –> too large

49
Q
  • when does placenta take over production of which hormone (that was initially secreted by corpus luteum)?
  • vs for cows? ewes? mare?
A
  • progesterone! after 2.5 months/after 1st trimester –> production will increase until parturition (graph)
    *time at which placenta takes over progesterone synthesis
  • cows: last 1-3 months of 9 months
  • ewe/sheep: by 50 days of 5-month gestation
  • mare/horses: by 70 days of 11 month gestation
50
Q

when is hCG detectable in urine?

A
  • not detectable in first week
  • by 14 days, detectable
  • peaks at around 8 weeks
  • then starts to decline = difficult to detect pregnancy after first trimester
51
Q
  • any steroids that are produced on maternal side can do what?
  • where can the steroids be metabolized?
  • specific enzymes for steroid synthesis are present where (3)
    vs enzymes needed to degrade and metabolize steroid hormones present where (3)
A
  • can crossover to the fetal side
  • adrenal gland of mother, placental cells and adrenal gland of fetus
  • placenta (?) + fetal liver and maternal liver
52
Q
  • why does placenta bring enormous changes in pregnant female?
A
  • because of placenta’s endocrine functions
53
Q

fertilized embryo, as it travels from fallopian tube to uterus, fertilized embryo is considered as a ____A_____ –> consequence?
- as a _____A_______, the fetal placental unit manipulates the maternal _________ via output of (2) hormones resulting in _________ changes

A
  • parasite! (foreign thing) = localized immune suppression
  • as a parasite –> manipulates maternal “host” via output of polypeptide and steroid hormones resulting in physiological changes
54
Q

what are 6 physiological changes that happen in the mother bc of placental endocrine secretions?
+ big change that occurs!

A
  1. increase in cardiovascular function (HR + 20%, cardiac output +20-30%)
  2. blood volume +50%
  3. pulmonary changes (tidal volume +30-40%)
  4. gastrointestinal (increased gastric emptying time, decreased sphincter tone)
  5. renal (flow +25-50% of glomerular filtration rate)
  6. body weight (uterus + 15x and fat accumulation)
    + change in term of mammary gland/breast
55
Q
  • when does changes in breast start?
  • which hormone stimulates duct formation and accumulation of fat in breast tissue?
  • effect of this hormone increases/decreases during pregnancy
  • source of this hormone?
A
  • 2 years before end of pre-puberty
  • estrogen!
  • increase during pregnancy!
  • source = ovary but MAINLY PLACENTA! during pregnancy
56
Q

which hormones does placenta produce that are necessary for milk production? (4)

A
  • estrogen
  • glucocorticoids
  • prolactin
  • placental lactogen (prolactin-like hormone)
    *prolactin and placental lactogen add to estrogen effect of mammary gland development
57
Q
  • what prevents milk production during pregnancy?
  • how does milk production start?
  • what signals prevent ovulation during lactation?
A
  • high concentrations of estrogen and progesterone
  • after partuition/birth, estrogen and progesterone levels fall, but prolactin stays high = milk production starts
  • during nursing, high prolactin inhibits GnRH = decrease gonadotropins = no follicle release for up to 12-17 weeks in humans
58
Q

what are the 3 big steps of mammary gland development?
- which hormones are involved?

A
  1. rudimentary = prepubertal development (8-9 yo) –> formation of alveoli, duct systems, growth
    - estrogen, progesterone, glucocorticoids, insulin, growth hormone and prolactin
  2. pregnancy –> full alveolar development, further branching and duct development
    - same 6 hormones –> estrogens, progesterone + chorionic mammotropin from placenta!
  3. lactation/post parturition
    - decrease in estrogen and progesterone + increase of prolactin + glucocorticoids + oxytocin for milk ejection
59
Q
  • parturition is 100% regulated by what?
  • what initiates parturition?
A
  • by hormones!
  • we don’t know exactly what begins it but we hypothesize that it’s the fetus that initiates the process –> fetus can double their weight in the last month of gestation –> leads to fetal stress/physical congestion
60
Q

describe the hormone pathway that leads to parturition
*3 important hormones!

A
  1. fetal stress –> increase fetal ACTH (adrenal corticotropic hormone –> stress hormone from the pituitary)
  2. fetal ACTH increases cortisol (steroid hormone)
  3. cortisol stimulates enzymes in placenta towards synthesis of estrogen (big increase in estrogen synthesis)
    3.1. estrogen increase leads to increase of myometrial contractions of the uterus (has been kept quiet throughout gestation bc of progesterone) + increase secretion from cervix and vaginal lining = lubrication
  4. cortisol also stimulate prostaglandin F2 alpha (PGF2a) (mainly synthesized in corpus luteum for its regression)
    4.1 PDF2s synthesized in corpus luteum for its regression = luteolysis +inhibits progesterone synthesis in placenta + stimulates myometrial contractions
  5. increase myometrial contractions (from E2 and PGF2) = increase pressure = increase cervical stimulation (opens up + also secretes mucus for lubrication) = increase oxytocin
  6. oxytocin + estrogen + prostaglandin –> put effect on myometrium = contractions increase rapidly = expulsion of fetus
61
Q

which 2 hormones regulate (stimulate/inhibits) myometrial contractions?

A
  • progesterone = inhibits myometrial contraction
  • estrogen = increases/stimulates myometrial contractions
62
Q

how does stimulation of cervix leads to oxytocin synthesis? 3 steps
- needs both (2) regulation

A
  • needs both neural and endocrine regulation
    1. contraction and movement of fetus towards cervix puts pressure on cervix –> sends neuronal signal through spinal cord to reach hypothalamus at PVN (paraventricular nucleus)
    2. PVN neurons produce oxytocin (from posterior pituitary)
    3. oxytocin secreted in circulation –> all the way to uterus to assist estrogen and prostaglandin to increase contraction and labor
63
Q

does parturition complete with expulsion of fetus?
- how does it complete?

A

no! it completes when placental membranes are expelled

64
Q

post-partum period –> also called what?
- maternal steroidogenesis return to normal levels within __-___ days
- pituitary gland increases in size by about ___ during pregnancy –> does not decrease in size until what?
- pituitary gland –> increase in __________ that produce _______ to support what?
- which hormone suppresses what to prevent ovulation?
- normal menstrual cycles resume in about ___ weeks

A
  • also called puerperium
  • 1-3 days
  • 1/3 –> does not decrease in size until lactation ends
  • increase in lactotrophs producing prolactin to support milk production
  • prolactin suppresses GnRH –> suppresses FSH/LH secretion = prevent ovulation
  • in about 17 weeks/4 months post parturition
65
Q

describe neurohormonal control of milk ejection (different from milk synthesis)

A
  1. suckling on teats/attachment of milk machine on teats initiates neuronal signaling –> pass through spinal cord to reach PVN
  2. PVN neurons secrete oxytocin
  3. oxytocin act on muscle cells surrounding mammary gland alveoli (epithelial cells of alveoli synthesize milk + secrete milk)
  4. milk is pushed into duct system –> come together to form teat canal –> milk ejection/production

Endocrinology (14 decks)

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