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Repro Flashcards

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1
Q

difference between sexual determination and differentiation

A

determination - genes (eg. being XX or XY) determined by SRY presence

differentiation - what sex your internal and external genitalia develops as

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2
Q

gonadal development

+ the 3 waves of cell invading genital ridge

A

genital ridge –> ovaries / testes depending on presence of SRY gene

  1. Primordial germ cells –> sperm/ oocytes
  2. Primitive sex cords –> Sertoli cells (SRY present) / granulosa cells
    - Sertoli cells –> AMH release
    - Granulosa cells –> required for conversion of androgens to E2 in menstraul cycle
  3. Mesonephric cells –> blood vessels/ leydig (SRY) / theca cells (no SRY)
    - Leydig –> testosterone release
    - Theca
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3
Q

what 2 ducts determine internal genitalia + the hormones that influence its development

A

mullerian ducts - female internal
develops if absence of AMH (sertoli) and Testosterone (leading)

wolffian ducts - male internal
develops due to presence of AMH / Testosterone

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4
Q

where is the SRY gene located

A

on the short arm (p)

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5
Q

why tissue is the genital ridges derived from

A

somatic mesenchymal tissue

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6
Q

what determines external genitalia differentiation

A

presence/absence of DHT

testosterone ——–5a-reductase—–> DHT

males and females both have this enzyme but testosterone only in males

DHT causes differentiation of male external genitalia

  • clitorial enlargement
  • labia fuses - scrotum
  • prostate forms

no DHT = female external differentiation

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7
Q

what receptors do DHT bind to

A

testosterone but they are more potent than testosterone

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8
Q

what is SRY

A

Sex determining region Y (SRY)

switches on during development
if it does not switch on - ovaries develop

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9
Q

what is gonadal dysgenesis

A

incomplete sexual differentiation

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10
Q

what is

  • androgen insensitivity syndrome
  • 5a-reductase deficiency
  • turners syndrome
  • congenital adrenal hyperplasia
A

all types of gonadal dysgenesis

AIS: testosterone is produced in males but faulty receptors
AMH is still present so wolffish ducts but failure/abnormal external male genitalia

5a-reductase deficiency: no DHT

  • normal internal
  • faulty external (eg. no descent of testis)

turners: missing/inactivated one X chromosome 45
- ovaries present
- but small/’streaked’ because you need 2 Xs for full ovarian development

CAH: female exposed to high levels of androgens

  • no testes as no SRY
  • but presence of both mullerian and wolffian ducts
  • external genitalia is male-like
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11
Q

explain the HPG axis

A
  1. kisspeptin to hypothalamus (inactive 145aa and cleaved into active forms - there are 4)
  2. hypothalamus releases GnRH associated peptide (GAP) 56aa which is cleaved by endopeptidases at processing site P to form decapeptide (10aa) = active GnRH

GnRH is released in a pulsatile way to pituitary (otherwise continuous, GPCR will decouple from 2ndary messenger systems)

  1. fast pulses–> LH from pituitary
    slow pulses–> FSH

due to GnRh being released in pulses, so are the gonadotrophins

  1. gonads produce testosterone/ progesterone/ oestrogen (can also negative feedback to hypothalamus / pituitary)
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12
Q

what is the similarity and difference of the 3 gonadatrophins

A

LH/FSH/hCG all have same alpha-subunit (92)
which is released in excess

but have different beta which is limited therefore limits hormone conc

  • LH: 121
  • FSH: 110
  • hCG: 145

also hCG is NOT produced by pituitary

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13
Q

2 major endocrine events of puberty

A
  1. ADRENARCHE
    - adrenal maturation (zona reticularis)
    - secretion of adrenal androgens (DHEA/DHEAS)
    - enter circulation to tissues where it can be converted into testosterone / DHT

first thing as a result of DHEA increase we see =
pubarche also occurs (growth of pubic/axillary hair)

increased sebum production (–> acne)

  1. GONADARCHE
    - reactivation of HPG axis (pulsatile release of GnRH)
    - epiphyseal growth- oestrogen (initial low conc: growth / high conc: epiphyseal fusion)
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14
Q

2 types of pilosebascous units

A
  1. Vellus PSU differentiate to either:
    - terminal- PSU: facial hair
    - APO-PSU: axillary hair
  2. Sebacous
    - large sebaceous gland
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15
Q

what is puberty

A

non reproductive —> repoductive
+
where secondary sexual characteristics develop (primary = at birth)

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16
Q

what is consance

A

smooth ordered progression of change

every child undergoes the same order of changes
but the onset/duration will vary

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17
Q

what typically is the first sign of puberty for girls/boys

A

girls: thelarche (breasts enlargement)
boys: testicular volume increasing >4ml

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18
Q

when does fertility ‘begin’ for boys/girls

A

girls: 1st year of period
boys: from beginning of puberty (as soon as HPG axis awakens because FSH—> Sertoli cells–> spermatogenesis)

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19
Q

2 types of precocious puberty

A
  1. CENTRAL
    - gonadotrophin dependent
    - consance is maintained
    - excess GnRH/gonadotrophin secretion
    - high FSH/LH/E2/Testosterone
  2. PERIPHERAL
    - gonadotrophin independent
    - consance is not maintained
    - low FSH/LH but high E2/testosterone
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20
Q

when is it considered delayed puberty

A

girls: >13yrs / >18yrs for menarche
boys: >14yrs

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21
Q

explain process of primordial germ cells in development of a foetus and the form they arrest in for girls until puberty

A
  1. if genital ridge–> ovaries
  2. PGC will enter become oogonia and differentiated into egg/oocytes
  3. mitosis (increase in number - but still diploid)
  4. meiosis begins
  5. BUT arrest in meiosis anaphase I = primary oocytes
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22
Q

folliculogensis

A

PRE-ANTRAL PHASE(gonadotrophin independent)
once puberty starts a few follicles will start growing
- multiplication of granulosa cells
- oocyte grows by synthesising protein
- thick protective layer = zona pellucida
2nd layer of basal lamina differentiates into theca cells

so layer around oocyte:
zona pellucida, granulosa cell, basal lamina (secreted by granulosa), theca cells

ANTRAL PHASE (gonadotrophin dependent)

  • follicle grows
  • fluid enters via gaps of granulosa = antrum
  • antrum pushes oocyte to the side
  • granulosa cell surrounding oocyte = specialised = cumulous cells

FOLLICLE RECRUITMENT

  • only follicles grown to right side will respond to FSH = recruited
  • continue growth
  • only one will be selected for ovulation –> grow massively (Graafian follicle)
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23
Q

what is the 2-cell 2-gonadtrophin theory

A

theca cells have LH receptors + are highly vascularised (blood supplies LH)

stimulates synthesis of cholesterol—-> androstenedione(androgens)

released around body

some to granulosa cells: androstenedione—-aromatase—> E2 (this process is driven by FSH)

oestrogen drives granulosa cells (positive) as well as negative feedback to HPG

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24
Q

aims of menstraul cycle

A
  • select single oocyte to be fertilised
  • regular spontaneous ovulation to maintain fertility
  • ensure correct no. of chromosomes in eggs
  • cyclical changes in vagina/cervix/utereus
  • preparation of uterus to receive a potential embryo + support it
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25
Q

2 phases of menstraul cycle

A

starts from first day of bleeding

  1. follicular phase
  2. luteal phase

luteal phase ALWAYS lasts only 14days
follicular phase can vary per woman

a regular period = within 4 days difference from last period

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26
Q

describe whole menstraul cycle

A
  1. CL dies
  2. progesterone falls = HPG axis inhibition is stopped
  3. rise in FSH
  4. recruitment of antral follicles that are of the right size/respond
  5. they produce a lot of oestrogen
  6. negative feedback
  7. decrease in FSH
  8. (window of opportunity) only the dominant follicle is able to survive the low FSH levels
    - more FSH receptors
    - LH receptors on granulosa cells
    - more granulosa cells - more E2 production - more negative feedback to decrease FSH for the others
  9. dominant follicle produces E2
  10. sustained levels of E2 for 2 days (>300) causes HPG to switch back on
  11. LH surge:
    - oocyte released
    - empty follicle –> CL
    - lutenisation of granulosa/theca

the oocyte will have undergone meiosis I in dominant follicle becoming a secondary oocyte (forming a 1st polar body with the other half of the chromosomes)

secondary oocyte will being meiosis II but will arrest again and only complete when fertilised (+create a secondary polar body containing identical sister chromatids)

  1. high progesterone from CL
  2. decrease in FSH/LH
    (we expect the oocyte to have ovulated + fertilised and so prevent other follicles growing)
  3. after 14 days, if no pregnancy, CL dies
  4. decrease in progesterone so cycle begins again
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27
Q

what receptors are on the corpus luteum (and therefore maintains it)

A

LH
hCG (if pregnant - trophoblast of embryo/blastocyte will produce)

the hCG has similar structure to LH so it binds to LH receptors

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28
Q

what are the 3 layers of uterus

A

perimetrium
myometrium –> circular/ figure of 8 spiral/ longitudinal
endometrium

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29
Q

what hormone determines the size of uterus

A

oestrogen

high oestrogen—> high proliferation /cell division –> expand

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30
Q

how does the follicular and luteal phase affect the endometrium

A

follicular (high oestrogen)

  • proliferation
  • cell division
  • glands expand
  • high vascularity

luteal (high progesterone)

  • differentiation / mature
  • cell division decreases
  • glands secrete glycoproteins/lipids
  • high vascularity –> oedema

at the end of luteal (decrease in progesterone) = menstruation

  1. endometrium releases prostaglandins
  2. constriction of vessels
  3. necrosis/hypoxia + proteolytic enzymes from necrotic tissue
  4. vessels dilate –> bleeding
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31
Q

name the parts of the uterine tube

A

fimbriae–> infundibulum –> ampulla –> isthmus

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32
Q

name the parts of the uterine walls

A 
outer= serosa
smooth longitudinal
circular muscle fibres
mucosa with 2 main cell types
- secretory: nutrients for early embryo
- columnar ciliated epithelium: to waft oocyte along down tube
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33
Q

how are uterine tubes affected by follicular/ luteal phase

A

follicular phase (high oestrogen)

  • differentiation
  • high secretions
  • ciliary cells waft
  • mucosa increases in height

luteal (high progesterone)

  • undifferentiation
  • stop cilia/secretion
  • decrease in height of mucosa
34
Q

2 ways of testing for blocked tubes

A
  1. laproscopy and dye
    (insert dye via cervix and insert laprocscope via abdomen to see if dye appears in pelvic cavity)
  2. hystero salpingo-contrast sonography
    (uterus with dye via vagina and use ultrasound to see if it makes its way to tubes)
35
Q

how does the follicular/luteal phase affect the cervix

A

mucosa:

FOLLICULAR (oestrogen)

  • less viscous mucosa
  • contains glycoproteins = aligned = microscopic channels = sperm can swim up the channels

LUTEAL (progesterone)

  • more viscous due to less secretions
  • mesh like glycoproteins to stop sperm
36
Q

describe spermatogenesis

A
  1. mitosis of spermatogonia to increase number
  2. there are 2 types:
    - A: that stay as sperm that will keep dividing via mitosis/ become B
    - B: commit to meiosis
  3. meiosis –> spermatocytes
  4. spermiogenesis (losing cytoplasm/elongation/movement of cellular components) –> spermatids
37
Q

where are leydig and Sertoli cells located within the testes

A

Sertoli cells = within seminiferous tubules

leydig = outside of seminiferous tubules (between them)

38
Q

where/what does seminal fluid receive secretions from

A
  1. bulbs-urethral gland
    - lubricates inside of urethra
    - neutralises acidic urine and friction
    - clear viscous, high in salt
  2. seminal vesicles - fructose energy
    - PG
    - vit C
    - enzymes
    - FRUCTOSE for energy
  3. Prostate - liquefaction later
    - milky white component
    - proteolytic enzymes
    - prostate specific antigen
39
Q

if semen does not liquefy later, what is the problem

A

prostate not producing the proteolytic enzymes

40
Q

what is a spermatozoon and describe 2 adaptations to help with its function

A

a mature sperm

mitochondria produces ATP –> axoneme fibres to slide against each other–> power to pull flagella –> propel sperm forward

acrosome at front of head
4-18hrs–> capacitation–> explodes and releases enzymes to help cut through outer layer of egg

41
Q

why can high oestrogen lead to DVT

A

oestrogen in the liver stimulates clotting factors

42
Q

why is the seminal fluid removed before undergoing capacitation

A

seminal fluid consists of inhibiting factors

43
Q

what occurs during capacitation

A

sperm gets closer to egg = alkaline environment

CatSper channels open (voltage gated cation channels set by pH)

ca influx

sperm gets hyperactivated

tail beats more forcefully (higher amplitude and frequency)

44
Q

what occurs during acrosome reaction

A

capacitation must occur before

  • when sperm is right next to the egg
  • acrosome will burst release hyalurondiase
  • this will digest the cumulus cells and corona radiata (digests hyaluronic acid)
  • sperm reaches zona pellucida
  • binds to ZP3 (human specific) triggering TRUE acrosome reaction
  • enzyme across digests zona pellucida and sperm enters oocyte
45
Q

what happens when sperm and oocyte fuse (syngamy)

A
  1. sperm nuclei falls into egg (tail is lost)
  2. sperm has special PLC-zeta (PLC–> PIP2–> IP3+DAG–> increase in Ca)
  3. triggers cortisol reaction –> releases enzymes to cleave adhesions molecules from sperm to stop polyspermy
    also triggers oocyte to complete meiosis II
  4. there are 2 pronuclei (maternal and paternal nucleus have own distinct membranes around nuclei) that will undergo DNA replication
  5. they will fuse
  6. mitosis so that each daughter cell has 46 chromosomes
46
Q

give the expected timeline for cell division after the 2 pronuclei fuse in the egg

A

after 3/4 days –> 6-8 cells = morula

after about 5 days –> 100 cells = blastocyst

blastocyst has a blastocele fluid cavity with a trophoblast surrounding it (this will become placenta)

47
Q

where is androgens (testosterone) produced

A

mainly testes

adrenal cortex (glomerulus reticularis)
adipose tissue
48
Q

what gonadotrophin controls leydig and Sertoli cells

A

LH - leydig

FSH - sertoli

Leydig cells will produce testosterone which will act on Sertoli cells for spermatogenesis to occur + AMH release

49
Q

mechanism of testosterone once entered in a cell

A

either:
bind to its nuclear receptor in the cytosol then
-growth of wolffian ducts —> internal male genitalia
-initiate spermatogenesis / maintain in adults

or
be converted to DHT (via 5a-reductase)
-binds to same testosterone receptor (but more potent)
-therefore amplification of testosterone action
-external genitalia differentiation
-sexual maturation
-puberty

50
Q

what are 5a-reductase inhibitors used to treat

A
  • prostate cancer

- balding

51
Q

2 types of 5a reductases

A

type I - scalp/skin

type II - genital skin/prostate

52
Q

what is danazol and cyproterone acetate and what are they used to treat

(uses of androgens/anti-androgens)

A

danazol = androgen derivative

  • feedback to decrease LH/FSH
  • but not converted into oestrogen
  • to decrease ovulation/breast tenderness(mastalgia) /menorrhagia (heavy periods)
  • endometriosis

cyproterone acetate = inhibits peripheral androgen receptors

  • precocious puberty
  • supress initial surge effects of goserelin and buserelin
  • acne
  • hiturism
  • virilisation in women
53
Q

what effects would you see if you gave GnRH agonists vs. GnRH antagonist analogues

A

agonists

  • initial LH/FSH increase
  • but will stay bound to GnRH receptor –> desensitise (needs to be pulsatile)
  • long term will decrease gonadotrophin
  • used to treat prostate cancer/endometriosis

antagonists

  • no initial LH/FSH increase
  • they just block the receptors
54
Q

primary and secondary hypogonadal syndrome

A

primary = HYPERgonadotrophic hypogonadal

  • testes failing to respond to LH
  • chromosomal abnormality: kinefelter syndrome (47XXY)
  • LH/FSH is high due to neg feedback from low/no testosterone
  • could give testosterone but risk of early epiphyseal closure (faltered growth)

secondary = HYPOgonadotrophic

  • pituitary failing to produce gondatrophin LH/FSH
  • kalmann’s syndrome (loss of smell = distinctive feature)
  • giving synthetic GnRH will take time until change is seen
55
Q

around how many days after ovulation does blastocyst enter the uterus

A

5/6

if too early –> no implantation
too late –> ectopic

56
Q

what happens after blastocyst reaches epithelium cells of endometrium

A

enzymes on endometrium help dissolve zona pelucida

trophoblasts invade —> synctiotrophoblast and cytotrophoblast

as synctiotrophoblast continue to invade there are 2 cell divisions occurring:

  • cytotrophoblast –> placenta
  • inner cell mass –> epiblasts and hypoblast –> 3 germ layer( ecto, endo and meso)

trophoblasts that down differentiate –> chorion and extra embryonic mesoderm

fluid filled sac–> yolk (circulation for first few days) + amnion (which later covers foetus –> amniotic fluid)

chronic villi form from embryonic mesoderm

endometrium has spaces = lacuna which will fill with maternal blood

57
Q

why do we use B-hCG to detect pregnancy

A

secreted by synctiotrophoblast to maintain CL during pregnancy (cl produces steroids oestrogen/progesterone maintaining the endometrium)

alpha-subunit is same as LH/FSH
but beta is different

58
Q

what hormonal changes are there with pregnancy

A

placenta

  • takes over steroid production from CL (progesterone/E2/E3)
  • peptides: hCG/hPL/GH

hPL –> insulin resistance

placenta also produces its own
-cortisol: foetal lung maturity/ mineralocorticoid action / insulin resistance

-CRH leading to increase of ACTH–> inc. DHEA–> inc. prostaglandins in uteroplacental tissues–> inc. BF + cervical contractions
(labour initiation)

pituitary

  • GH
  • thyroid
  • prolactin (suckling increases it; progesterone inhibits it)
  • corticotrophin releasing hormone
59
Q

what contributes to weight gain with pregnancy

A
  • foetus and placenta
  • fat + protein
  • breasts
  • uterus

water gain
- placenta renin –> increases RAAS

E2 –> unregulated angiotensin synthesis in liver
however preg. women are resistant to AT2 receptor so decrease in vasoconstriction
(RAAS- constriction)

  • E2/Prog act as mineralocorticoid–> increase sodium retention –>increase Blood volume
  • connective tissue/ligaments take on water and become softer
  • resetting osmostat - lower threshold –> drink more
60
Q

why is there an increase in o2 consumption with pregnancy

A

CO2 sensitivity increases + anatomy change of ribcage more out–> breathing more/deeply–> minute volume increases–> high arterial O2 and lower pCO2 —-> steeper gradient for gas exchange

61
Q

how is CVS affected with pregnancy

A
  • expanding uterus pushes on heart –> change in sounds and ECG
  • E2–> NO–> peripheral vasodilation –> dec. TPR—> increase in perfusion of uterus/placenta/kidney/skin etc
  • neoangiogenesis and increase in skin capillaries(spider naevi) to increase heat loss

pregnancy = LOW pressure, HIGH volume

62
Q

GI changes with pregnancy

A
  • increases in appetite/thirst
  • dec. GI motility –> constipation
  • reduced LOS –> acid reflux

best to eat small frequent

folic acid supplements (400ug/day until week 12) –> DNA production/growth/blood cells for uterus/placenta/fetus

63
Q

urinary system changes with pregnancy

A
  • pee more as baby pushes on bladder
  • CL/placenta release relaxin —> formation of endothelin–> dilation of renal arteries via NO–> UTI risk
  • progesterone/VEGF–> inc. resistance to Ang II–> dec. vasoconstriction –> inc. BF to kidney –> inc. in GFR
64
Q

what do you see when “returning to normal” after a pregnancy

A

Dramatic and rapid fall in steroids on delivery of the placenta.

Most endocrine-driven changes return to normal rapidly.

Uterine muscle rapidly looses oedema but contracts slowly: never returns to pre-pregnancy size.

Removal of steroids permits action of raised prolactin on breast.

65
Q

why does menopause occur?

A

reduced follicle count
-also normally granulosa cells secrete small amount of AMH which inhibits FSH therefore decreasing recruitment of follicles but as you age less granulosa cells=less inhibition = more follicles lost via recruitment

reduced granulosa cells/function

  • as you age they become less effective at producing oestrogen
  • less inhibin A and B to suppress FSH

increased chromosomal abnormality of oocyte

  • so decreased ability to repair DNA
  • increase aneuploidy risk
66
Q

what is clomiphene

A

drug used to help follicle recruitment (release)

67
Q

what causes shortened cycle(initial) and delayed ovulation/absence in menopause

A

shortened cycles

  • decrease in inhibin B which normally prevents follicular phase
  • so you get high oestrogen and LH surges earlier

delayed/absence

  • despite high FSH
  • faulty granulosa cells
  • oestrogen rise is not high enough to induce LH surge
  • no ovulation
68
Q

why might you get constant heavy bleeding with menopause

A
  • despite high FSH
  • faulty granulosa cells
  • oestrogen rise is not high enough to induce LH surge
  • no ovulation
  • so dominant follicle not recruited/released
  • no progesterone produced - constant bleeding?
69
Q

why are UTIs common for pregnant women

A
  • in hospital more = higher diagnosis rate
  • high progesterone –> SM relaxation –> urinary stasis –> more likely to be infected
  • pregnant women have lower immune system (to prevent attacking foetus)
70
Q

problems that can arise if mother is hyperglycaemic for foetus

A
  • sacral agenesis (sacrum doesn’t form) risk
  • Congenital heart disease risk
  • skeletal malformation risk
  • inhibits surfactant production –> resp distress on delivery risk
  • neonatal HYPOglycaemia (foetus will produce high insulin but after birth the insulin is too high for glucose in its own blood)
  • glycosuria as high glucose–> increases water out of intestitium–> peeing alot–> increase amniotic fluid (polyhydramnios–> uncomfortable for mum
  • hypoxic–> jaundice
71
Q

4 high BP pathology classifications

A

<20weeks

  • pre-existing HT (no proteinuria)
  • pre-existing HT due to RENAL disease (proteinuria)

> 20weeks

  • pregnancy induced HT (no proteinuria)
  • Pre-clampsia (PET) (proteinuria)
72
Q

why do you get PET

A

peripheral vasodilation fails so high TPR due to vasoconstriction/vasospasm

most likely due to failure of 2nd wave of trophoblastic invasion at 15/16weeks so normal dilation of vessels do not occur/develop

73
Q

stages of labour

A
  1. contractions—> dilation 10cm
    - latent phase: up to 3cm + PGs to inc. permeability in cervix for collagen breakdown/soft
    - active phase: up to 10cm (1cm/hr)
  2. dilation–> delivery of foetus
    - rotation of baby head past pelvic inlet
    - delivered with facing mothers back
    - rotation for shoulders to come out
  3. removal of placenta
    - in thigh SYNTOMETRINE (artificial oxytocin and ergometrin)
    - umbilical cord is clamped to prevent getting into baby
    - placenta dettaches
    - check by feeling pubic symphsis

labour complete after placenta has been delivered

74
Q

what is dystocia

A

despite uterus contracting normally

the baby does not exit due to physical block

75
Q

which hormone increases contraction and which decreases

A

oestrogen - increases

progesterone - decreases

76
Q

stimulation of which ANS receptors increases/decreases contraction of myometrium (uterus)

A

a1 - increases contraction

b2 - decreases contraction (relaxes)

77
Q

describe the myogenic contraction mechanism of uterus

A
  1. interstitial cells of canal initiate slow wave activity
  2. depolarisations of these causes AP
  3. AP runs down from ICC to SM cells via gap junctions

oestrogen increases the gap junctions–> easier coordination/contractiosn

  1. SM contraction via PLC/inc. Ca/MLCK pathway
78
Q

why might hypertonus occur (uterus)

A

too much contraction over relaxation

high conc of ca in cell than it is being extruded out
therefore incomplete relaxation

79
Q

why does increasing contraction of uterus treat haemorrhage

A

contracting uterus/ligature decreases bleeding

eg. oxytocin

80
Q

increase in oestrogen increases the synthesis of which 2 types of prostaglandins

A

PGE2 = vasodilator

PGF2a = vasoconstrictor

but both have an effect to increase myometrium contraction

81
Q

why might it be better to use prostaglandins vs. oxytocin to increase contractions of uterus

A

oxytocin is dependent on oestrogen

low oestrogen = low oxytocin + low oxytocin receptors

however, there are always many prostaglandin receptors

82
Q

myometrium relaxants for premature birth

A
  • B2 adrenoceptor agonists (salbutamol) they increase PKA
  • ca2+ channel antagonists (nifedipine/mg sulfate)
  • oxytocin receptor antagonists (retosiban)
  • COX inhibitors (NSAIDs)

Semester 4 (10 decks)

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