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Vets6108* > Female Repro Physiology > Flashcards

Female Repro Physiology Flashcards

1
Q

What is GnRH?

A

FSH + LH

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2
Q

What is the function of FSH?

A
  1. stimulate follicular growth in females
  2. Stimulate sertoli cells in males (thus spermatogenesis)
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3
Q

What is the function of LH?

A
  1. Induces ovulation of mature follicles
  2. Stimulates CL to produce progesterone
  3. Stimulates testosterone production in males
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4
Q

Where is Inhibin produced in male?

A

sertoli cells (regulate spermatogenesis)

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5
Q

Where is Inhibin prodeuced in female?

A

Tertiary follicles (target pituitary to inhibit release of FSH)

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6
Q

What is the function of oestrogen (E2)?

A
  1. increased uterine blood flow
  2. growth of uterine endometrial glands
  3. increased secretory activity of oviducts
  4. increased smooth muscle motility
  5. sexual receptivity (sexual behaviour)
  6. closure of epiphyseal growth plate in bones
  7. mammary duct growth
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7
Q

What is the function of P4?

A
  1. increased uterine endometrial gland growth
  2. increased secretory activity of endometrial glands
  3. inhibition of GnRH release
  4. mammary lobuloalveolar growth
  5. quiescence of uterus
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8
Q

Describe the HPG axis of male.

A
  1. Tonic center (hypothalamus) release GnRH in slow pulses > favouring FSH release
  2. LH activates T secretion from Leydig cells
  3. FSH activates the conversion of T to DHT (dihydrotestosterone) in Sertoli cells.
  4. sertoli cells also secrete In, inhibiting GnRH secretion in AP
  5. T exerts negative feedback on the hypothalamus, inhibiting GnRH release until T in blood drops.
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9
Q

what is follicular phase?

A
  • phase between the regression of CL and ovulation when follicles grow and mature
  • consists of pro-oestrus and oestrus stage
  • dominated by E2 > LH surge (prepares for fertilisation)
  • The longer the follicular phase, the higher the fertility.
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10
Q

What is the characteristics of oestrus?

A
  1. Anatomical/ histological changes
    - reddened vulva
    - opened cervix
    - cornification of vaginal epithelium
  2. cevical mucus changes
    - muscus thins and pH falls to avoid vaginal lubrication for copulation and spem transport
    - mucus: thick > luteal phase/ long string > oestrus (sex time)
  3. Fertility
    - ovulation is normally associated with oestrus
  4. Mating behaviour
    - mate seeking
    - courtship
    - acceptance of male
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11
Q

What is luteal phase?

A
  • stages between ovulation and regression of CL
  • consists of metoestrus and dioestrus
  • CL secretes P4 which is essential for maintenance of pregnancy and exerts negative feedback on pituitary to restrict gonadotrophin
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12
Q

what changes will have when it reaches the end of luteal phase?

A

P4 level drops and leading to a new follicular phase

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13
Q

Formation of corpus luteum.

A
  1. preovulatory follicle
    - fusion of theca interna and granulosa cells due to the break down of follicle
  2. Corpus haemorrhagicum
    - small vessels rupture
    - follicle implodes and fold inwards on itself
  3. Functional corpus luteum
    - large luteal cells: granulosa
    - small luteal cells: theca
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14
Q

Mare’s seasonal polyestrus cycle

A

with double wave of FSH as they need the extra progesterone to maintain pregnancy.

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15
Q

Mouse and rat cycle

A
  • Mating triggers the formation of corpus luteum
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16
Q

Queen’s cycle

A
  • will not ovulate if no physical stimulation (penile spine on the tip of the penis)
    If no mating- metoestrus and dioestrus are replaced by postoestrus (no CL formation)
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17
Q

Define induced ovulators

A
  • continuos follicular waves give constant high E2
  • mating induces ovulation- either from mechanical or chemical stimulation.
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18
Q

What is reproduction dominated by?

A

powerful negative feedback of sex steroids

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19
Q

factors regulating breeding season.

A
  1. Proximate (obligatory e.g. day length / modifying e.g. temp, nutrition)
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20
Q

what is anestrus

A

long photoperiods (spring/summer)

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21
Q

what is cyclicity

A

short photoperiod (fall/winter)

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22
Q

what is the steps for fertilisation?

A
  1. deposition of sperm
  2. capacitation of sperm
  3. ovulation of viable ovum (a)
  4. transport of ovum (a)
  5. meeting of viable sperm and viable ovum (a)
  6. acrosome reaction
  7. polyspermy block
  8. decondensation
  9. pronuclear formation
  10. syngamy
  11. cleavage
23
Q

describe vaginal depositors

A

small volume, high concentration, rapid deposition ejaculate.

24
Q

describe uterine depositors

A

large volume, low concentration, slower depoisition ejaculate

25
Q

How do sperm be transported to the ampulla?

A
  1. Rapid transport is helped by the contraction of the uterus - swimming keeps spermatozoa in suspension
  2. beating of cilia in fallopian tubes may help
  3. oestrogen (follicle) stimulates an increase in uterine contractility and increases cervical mucous amount and fluidity.
  4. oxytocin (posterior pituitary & seminal plasma) stimulates smooth muscle contractions

(*But prostaglandins cause deterioration of cervical mucus)

26
Q

how do sperm prepare for fertilisation?

A
  1. Capcitation
    - destabilisation of sperm membrane (via cholesterol efflux)
    - influx of calcium
    - reversible phenomenon
    - preparation for acrosome reaction
  2. binding to oviductal epithelium
  3. acrosome reaction
    - decondensation of acrosome
    - release of enzyme
  4. sperm motility
    - changing to thrashing motion (hyperactivation)
27
Q

Describe the steps of ovulation and ovum transport.

A
  1. ovulation occur randomly on the ovarian surface (except in the horse)
  2. oocytes must be picked by the fimbria and guided into the oviduct, aided by the cumulus oophorus and corona radiata
  3. beating of cilia moves the oocyte along the ampulla
28
Q

what is syngamy?

A

the fusion of male and female pronuclei.

29
Q

preimplantation losses

A
  1. if the embryo is lost prior to the antiluteolytic signal then subsequent oestrus will occur at normal time (as if conception never occured)
  2. if female is late in return to oestrus, it can be assumed there was conception followed by embryonic loss
  3. litter bearing animals tend to ovulate more embryos than the uterus can carry so there must be embryo loss
  4. polytocous species have minimum number of embryos (~4) for establishment of pregnancy.
  5. normally, failure to conceive at one oestrus is NOT strongly correlated with failure to conceive at subsequent oestrus (es).
30
Q

What is the cause of pre-implantation loss?

A
  1. fertilisation failure
    - non0functional spermatozoa or a fault with the oocyte.
  2. genetic
    - a fault with zygote/ embryo during replication
  3. Physiological
    - maternal environment fails to support embryo due to faulty in the endocrine system or other pathology
31
Q

What destroys Cl? Where does it be produced?

A

(i) PGF2a
(ii) uterus

32
Q

Describe the embryo signal in ruminants.

A
  1. IFN-T produced by blastocyst
  2. IFN-T stops OTr synthesis (no PGF2a produced > corpus luteum not breaking down)
  3. IFN-T causes uterine protein production to promote the conceptus
33
Q

Describe the embryo signalling in pigs.

A
  1. E2 (estradiol) changes the way where PGF2a is released.
  2. PGF2a is diverted to the uterine lumen instead of uterine vein (minimal access to circulation )
  3. CL maintained
  4. E2 also causes myometrial contractions to distribute embryos within uterus.
34
Q

describe embryo signaling in horse and eCG.

A
  • conceptus secrets proteins that suppress uterine PGF2a production
  • eCG produced by the chorion maintains the production of P4 via formation of accessory CL
  • Increases in P4 when primary CL is formed
  • In pregnant animals, P4 starts to drop. Not until when animals start to produce eCG, it stimulates the production of P4. It also stimulates the secondary FSH waves which further causes the formation of corpus luteum and produce more P4
35
Q

Why is the fetus (embryonic) not being rejected as a foreign body?

A
  1. trophoblast cells produce factors (e.g. P4 and IFN-T) which acts as immunosuppressants
  2. trophoblast cells are coated with sialomucin (block binding) and have fewer histocompatibility antigens
  3. the trophectoderm is continuous and may act as dialysis membrane to keep fetal and maternal proteins separated
  4. the number of uterine leukocytes decreases in pregnancy
  5. the uterus secretes factors that act as immunosuppressants (e.g. PGE2 and transforming growth factor; TGF-B)
36
Q

what is placenta?

A

A transient endocrine and metabolic organ
- pregnancy maintenace
- mammary gland development
- fetal nourishment

37
Q

What is the transport across th eplacenta?

A
  1. gas via diffusion
  2. glucose partially metabolised into lactate
  3. amino acids actively transported (by placenta)
  4. fatty acid and immunoglobin transport highly species specific
  5. maternal lipids and hormones are blocked
  6. many drugs (e.g. opiods), bacteria and viruses can cross the placenta.
38
Q

state the efficiency of Ig transfer via diff placenta:
(i) epitheliochorial
(ii) endotheliochorial
(iii) haemochorial

A

(i) -
(ii) +
(iii) ++

39
Q

state the efficiency of Ig transfer via colostrum:
(i) epitheliochorial
(ii) endotheliochorial
(iii) haemochroial

A

(i) +++
(ii) ++
(iii) +

40
Q

What are the factors affecting foetal growth?

A

maternal:
1. maternal age
2. maternal size
3. maternal nutrition
4. climate e.g. high temp
5. litter size (polytocous species > larger litter size > compete for resources/ twins)

Fetal hormones:
1. thyroid hormones e.g. T4, T3 (required in sheep and monkey)
2. insulin from the pancreas
3. growth hormone (somatotrophin) from the anterior pituitary
4. somatomedins (mediators of somatotrophin)

41
Q

state the foetal-maternal interaction.

A

Foetal system profoundly affects mother:
- increased cardiac output (compensate for increased maternal CO2)

  • increase renal filtration rate (compensate for increased waste products in blood)
  • changes in metabolism (e.g. fat storage in 3rd trimester)
  • behaviour changes
  • endocrine changes (e.g. decrease E2 to foetal use)

Maternal endocrine system doesn’t directly affect foetus

42
Q

Initiation of parturition.

A

foetal cortisol (stress hormone) leads to:

(i) reduce placental P4 > increase E2 (increase myometrial contraction & lubrication)

(ii) produce PGF2a > luteolysis > reduce P4

(iii) PGF2a produce relaxin > pelvic ligament stretching

43
Q

List the periparturition hormones.

A
  1. cortisol- triggers parturition cascade
  2. P4 levels drop dramatically prior to parturition
  3. E2 increase sensitivity of the myometrium to oxytocin
    - reverse P4 induced uterine quiescence
    -relaxes the cervix by restructuring/ removal of collagen
    - stimulate PGE2 production by placenta
  4. PG (prostaglandin) stimulates myometrium contraction and expulsion of foetus (in conjunction with oxytocin)
    - causes luteolysis
44
Q

where is oxytocin be produced?

A

oxytocin is produced in hypothalamus but stored in posterior pituitary

it is also produced by the corpus luteum

45
Q

why is oxytocin being released? what is the stimuli?

A

pressure on the cervix

46
Q

describe the process of uterine involution

A

Return of the uterus to pre-pregnant state.

  • stimulated by prostaglandins and oxytocin
  • decrease in size and weight via vasoconstriction and muscle contraction
  • discharge of lochia
  • repair of tissue
47
Q

what is the composition of milk?

A

milk is an emulsion of fat globules with casein micelles (containing casein, calcium and phophorus) and leukocytes suspended in the aqueous phase, which contains solubilised lactose, whey proteins and minerals ie fat, protein, carbohydrates, vitamins, minerals and immunoglobins.

(plus whatever else in the blood of the mother- hormones, toxins, viruses)

48
Q

what is the major form of fat in milk?

A

primarily triglycerides
(secreted from mammary epithelial cells as fat globules)

49
Q

what are the proteins that can be found in milk?

A
  1. casein
  2. Whey proteins
    - a-lactalbumin: milk synthesis protein
    - b-lactalbumin
50
Q

carbohydrates content differs between species

A

monotremes: fucosyllactose (fucose + lactose)

marsupials: galactose (from glucose)

eutherians: lactose (glucose and galactose)

51
Q

How do milk be produced?

A

Stimulation: sucking

  1. prolactin binds to prolactin receptor > milk secretion

during pregnancy: progesterone bind with prolactin receptor and leads to low or no a-lactalbumin > low secretion

52
Q

What is the steps of milkf ejection reflex?

A

(i) suckling stimulates neural effect > trigger the release of oxytocin from the posterior pituitary

(ii) oxytocin is released to the mammary gland

(iii) oxytocin has an effect on myoepithelial cell around alveoli > cells contract and milk stored in it is squeezed out

53
Q

what is the relationship between udder pressure and milk secretion rates?

A
  • there is an inverse relationship between udder pressure and milk secretion rates
  • cessation of lactation (drying up of milk) happens when milk is secreted at a constant rate but is removed infrequently
  • if milk is not removed (weaning), there is a build up in mammary pressure, so a decreased uptake milk precursors (especially glucose) into the mammary gland
  • when no milk is removed, mammary involution occurs.
54
Q
A

Vets6108* (10 decks)

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