W1L3 Thu Female reproduction: hormone and cycles Flashcards

1
Q

What is oestrous vs oestrus

A
  • Oestrous is an adjective e.g.: an oestrous cycle
  • Oestrus is a noun e.g.: that cow is in oestrus (heat)
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2
Q

What is progestin

A

synthetic progestagens

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3
Q

Ovarian follicular development

A

-from 1 million to 2 million primordial follicles the female are born with, some are recruited via hormone and start to develop
-It can takes months for primordial follicles to develop into primary follicles
-primarry follicle are filled in the granlosa, antrum formation
-selection and dominace and finally ovulation
- Antral follicle growth are faster due to present of gonadotrophin receptor
- follicles are loss throughout the process, turning into atresia

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4
Q

what determine which follicle will be selected

A

-the fastest growing follicle will win, LH receptor can also appear in the granulosa cell, inhibin turn off FSH production, normal granulosa cell does not have LH receptor, only FSH receptor will die due to this

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5
Q

Follicular development stage of follicles and their characteristic

A

-Primordial follicles: quiescent (can stay dormant for a long time), continual atresia but lots recruited so high loss
-Recruited follicles: no turning back, low rate of atresia
-Gonadotrophin responsive: FSH and LH affect development, some atresia
-Gonadotrophin dependent: atresia if FSH too low, high rate of atresia
-Dominant follicle(s): ovulates with LH surge without LH > atresia

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6
Q

the two phase of ovarian cycle

A

-Follicular phase is oestrogens dominat. LH surge lead to ovulation
-Luteal phase is progestagens dominant, ending with luteolysis (luteal regression)

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7
Q

Ovarian Steroids precusor

A
  • cholesterol is the precursor, came from our diet for mammals
    -cholesterol is converted into progestagens, and then androgen and then oestrogen
    -cholesterol converted into pregnenolone via cholesterol side cleavages
    -aromatase convert androstenedione into oestrone
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8
Q

Ovarian Endocrinology of follicle and corpus luteum

A
  • Antral follicle
    – Stimulated by Gonadotrophins (FSH & LH)
    – Oestrogens (Oestradiol-17β)
    – Inhibin produced (-ve feedback)
  • Corpus Luteum (CL)
    – Stimulated by Luteotrophins (LH, PRL, hCG)
    –make Progestagens (oestrogen – some species)
    – Oxytocin store and produce in granulosa cell, for destroying CL
    – Luteolysis (Prostaglandin F2α) use to dedonating oxytocin
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9
Q

Oestrogen Production: Two-cell Theory

A

Theca cells: Cholesterol → Androgens
§ Obtain cholesterol from blood (theca interna is vascularised)
§ LH binding aids conversion of cholesterol → androstenedione
§ Androstenedione → testosterone
Granulosa cells: Androgens → Oestrogens
§ Androstenedione passes into granulosa cell (through basement membrane)
§ Androstenedione → oestrone → oestradiol-17b aided by FSH binding
§ Testosterone passed from theca cells directly → oestradiol-17b
§ Oestradiol released into BVs to communicate with brain or act locally on egg
§ Produce inhibin which is released into blood

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10
Q

Phases of oestrus Cycle

A

Pro-oestrus
– Growing follicles
– Oestrogen dominant
Oestrus (in heat)
– Large follicle
– High oestradiol
– Receptive to mating
– Ovulation (spontaneous or induced)
Met-oestrus
– CL forming
– Decreasing oestradiol; Increasing progesterone
Di-oestrus
– Active CL
– Progesterone dominant
– Luteal phase / Pseudopregnancy
Anoestrus
– Cessation of ovarian cycles
– Season, pregnancy, lactation, old age, illness or stress

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11
Q

Corpus luteum makes progesterone

A

LH surge > ovulation
* Ruptured follicle wall
* Angiogenesis
* Theca transforms and enters centre → small luteal cells (progesterone) 20%
* Granulosa transforms →large luteal cells ( progesterone, Oxytocin)

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12
Q

Rat/ mouse/ hamster ovarian cycle

A

Short 4-5 day cycles, ovulate spontaneously, CL regresses rapidly
§ If mated: cervical stimulation → surge of prolactin → prolongs life of CL (potential for pseudopregnancy)
§ Cycle strongly influenced by diurnal lighting pattern

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13
Q

Rabbit and cat ovarian cycle

A

Induced ovulators: no luteal phase unless mated
§ Follicles mature + persist (permanently ready to ovulate or in oestrus)
§ Cervix stimulation → LH release → ovulation → form CL
§ LH surge that causes ovulation responsible for pseudopregnancy

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14
Q

Sheep/ cow ovarian cycle

A

Follicular waves: 2 waves of follicle growth allowing ovulation to
occur more quickly should previous cycle not be successful
§ 2nd follicle will not ovulate due to high [progesterone]
§ CL present (progesterone) = atresia
§ No CL/atretic CL = maturation + ovulation

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15
Q

Active Luteolysis

A

s Action of prostaglandin F2a (PGF2a)
§ PGF2a produced by uterus endometrium on side of ovulation
- Rapidly metabolised in peripheral circulation (lungs)
- Local transfer of PGF2a from uterine venous drainage to ovarian artery via countercurrent transfer → directly to CL
§ Oxytocin from pituitary stimulates further PGF2a release from uterus(+ve feedback on PGF2a in uterine venous drainage)
§ Mechanism: 10-12 days in, CL downregulates its receptor → ↓progesterone → new follicles to grow + ↑oestrogen
→ release of oxytocin from pituitary → stimulates oxytocin receptors in uterus → PGF2a release
§ Structural Luteolysis: breakdown of CL by ↓blood supply to CL (TFN-a)
§ Functional Luteolysis: stops progesterone production pathway + stimulates cytokines (endothelin-1)

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16
Q

Passive Luteolysis

A

Withdrawal/inadequate luteotrophic support (LH)
§ After LH surge, low levels of LH maintain CL for 10-12 days
§ Embryo releases hCG/CG to maintain luteotrophic support + block luteolysis
§ No embryo = change from PGE (luteotrophic) to PGF2a (luteolytic) → oxytocin
§ PG (protagladin) has no effect unless in high concentrations