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REPRO2 > Infertility in the female > Flashcards

Infertility in the female Flashcards

1
Q

What are the main causes of infertility?

A
  1. Aberrant development of the genitalia
  2. Irregular or abnormal oestrous cycles
  3. Vulvar or vaginal discharge
  4. Failure to become pregnant
  5. Embryonic death
  6. Miscellaneous
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2
Q

List some examples of congenital and developmental anomalies of infertility in the female.

A

Largely structural

  • Ovarian hypoplasia
  • Reproductive tract dysplasia
  • Freemartinism
  • Inter-sex
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3
Q

What is ovarian hypoplasia?

A

When one or both ovaries are absent.

Virtually no follicles, no cycle, no oestrus.

Often bilateral, flaccid uterus.

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4
Q

What is the treatment for ovarian hypoplasia?

A

None

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5
Q

What does ovarian hypoplasia commonly occur in?

A

Swedish Highland cows

Mares with XO chromosomes

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6
Q

What is reproductive tract dysplasia?

A

Segmental dysplasia of paramesonephric ducts.
Developmental obstruction.
Ovaries function normally

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7
Q

What does a persistence of hymen (mare) result in?

A

bulge from vulva and strain at service

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8
Q

What is free-martinism/ how does it occur?

A

Vascular anastomosis of adjacent chorioallantoic sacs of heterozygous fetuses. Female becomes masculinised.

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9
Q

What are some of the features of the reproductive tract in free-martinism?

A
  • Prominent clitorisis hairy vulva
  • Paramesonephric ducts absent or grossly hypoplastic
  • ovaries vestigial and/or masculinarised
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10
Q

How do you diagnose free-martinisim

A

Failure to detect cervix

Sex chromosome chimerism

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11
Q

What species does free-martinism occur in?

A

95% of female with male twins in cow

Also occurs in goats

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12
Q

What is inter-sex?

A

Intersex encompasses developmental abnormalities resulting in discordance between genetic, gonadal or phenotypic sex.

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13
Q

What are some of the chromosomal abnormalities in inter-sex?

A
  • Default to develop female - SRY gene on the Y chromosome
  • XX: male pseudohermaphrodite
  • XO: Turners syndrome
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14
Q

How do you diagnose inter-sex

A

Karotyping

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15
Q

What is the incidence of inter-sex?

A

Relatively common in pigs (0.1-0.6%), goats and some dog breeds (American Cocker Spaniel)

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16
Q

What is Anovulatory anoestrus

A

Lack/cessation of cyclicity - delayed post partum or season. Associated with NEB

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17
Q

What is the incidence of anovulatory anoestrus?

A
  • Common in dairy cows (especially high yielding)
  • Prolonged anoestrus in bitches (>5-7mo)
  • Sows (associated with MMA)
  • Pregnancy failure in mare

NB mare in transition period has irregular oestrus and this is NORMAL

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18
Q

What is the clinical presentation of anovulatory anoestrus?

A

Failure to detect oestrus
(e.g. NSB, ONO)

Small, inactive ovaries
i.e. no dominant follicle or CL

Irregular progesterone profile

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19
Q

What are the pre-disposing factors for anovulatory anoestrus?

A 
Nutrition / body condition score
Stress
Lameness
Animals that are still growing
Suckling/maternal bond
Hormonal treatments
Endometritis
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20
Q

What are the two underlying endocrinologies of anovulatory anoestrus

A

Aberrant LH (and FSH) pulsatile secretion

Low insulin/ insulin-like growth factor 1 levels

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21
Q

What is the treatment for anovulatory anoestrus?

A

A combination of GnRH and progesterone.

GnRH stimulates FSH and LH which stimulates follicles to grow.

Progesterone will mimic the luteal phase, therefore withdrawl of P4 will stimulate the follicular phase to begin.

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22
Q

What is cystic ovarian disease?

A

Follicular structures that have failed to ovulate. Persistent, large follicles.

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23
Q

What are the different types of cystic ovarian disease?

A

Follicular- thin walled, under influence of oestrogen –> nymphomania

Luteal- partial luteinised; thickened wall, not ovulated, persistent structure –> anoestrus

24
Q

What is the incidence of cystic ovarian disease?

A

Common in cows (6-20%) and sows (5-10%) but very rare in mare, ewe, bitch and cat

25
Q

What is the pathogenesis of cystic ovarian disease?

A

Hormonal insuffieiciency- not producing enough LH, this may be because:

  • surge centre not producing enough GnRH or LH
  • Follicle does not grow efficiently, do not get enought estradiol production
26
Q

How do you diagnose cystic ovarian disease?

A
  • ultrasound: differential based on thickness of wall, always check both ovaries, normal CL can have thin walls
  • plasma/milk progesterone e.g. >2ng/ml: luteal

Accurate diagnosis is difficult

27
Q

What are the predisposing factors of cystic ovarian disease?

A
  • Treatment of underlying cause
  • Immediate post-partum period
  • Stress
  • Concurrent disease- Ketosis, uterine infections, mastitis
  • Breed (e.g. common in Holstein; rare in beef breeds)
28
Q

What is the treatment of cystic ovarian disease?

A
  • most spontaneously recover
  • Hormonal (single or combination)
  • Likely to re-occur
  • Avoid manual rupture
29
Q

What are the hormonal treatments for cystic ovarian disease?

A

-GnRH/ hCG (follicular) - causes follcile to lutenise, then remove luteal structure with PG
-Progesterone (follicular)
- Prostaglandin (luteal
)

30
Q

What is a prolonged CL?

A

Failure to return to oestrus . CL persists in absence of pregnancy.

Can occur in unmated animals.
Early Post-Partum period
Secondary endometrial problems

31
Q

What are the causes of prolonged CL?

A 
Failure to produce endogenous PG
Dioestrus ovulation (mare)
32
Q

What is the treatment for prolonged CL

A

PGF2a

33
Q

What is the incidence of prolonged CL

A

Common in the mare (20% of cycles)

Less common in the cow (2%)

34
Q

What does a granulosa cell tumour produce?

A

Oestrogens/ androgens

35
Q

What is the behaviour of granulosa cell tumours

A

Generally benign with infrequent metastasis

36
Q

What is the contra-lateral ovary like with granulosa cell tumours

A

Often small

37
Q

What hormones are elevated in granulosa cell tumours

A

Plasma testosterone/ inhibin

38
Q

What do granulosa cell tumours look like ultrasonographically?

A

Enlarged ovary with multiocular appearance

39
Q

What is the prognosis of granulosa cell tumour?

A

Good with removal

40
Q

What are some examples of veneral pathogens?

A

Bovine venereal campylobacterosis
Infectious pustular vulvovaginitis (IPV/IBR)
Contagious equine metritis

41
Q

When does metritis, endometritis and pyometra occur?

A

Post partum period (associated with retain fetal membranes)

Post mating (mare) - anatomic barrier integrity or following dioestrus

42
Q

What are the treatment options for metritis, endometritis and pyometra?

A

Abs can be effective
Lavage
Prostaglandin, oxytocin encourage contractions to expel the infection

43
Q

What is the incidence of metritis, endometritis and pyometra?

A

Cows (10-15%), Also occurs in mares and dogs

44
Q

What can be given (at the next mating) if there is a failure to establish pregnancy?

A

No product licenssed.
Stimulate progesterone production (GnRG/hCG)

Supplement with P4 - little evidence for benefit in mares

45
Q

What are some examples of acquired adhesions (reproductive tract lesions)?

A

Ovario-bursal

Hydrosalphinx

46
Q

What occurs with repro tract adhesions

A

Lumen is occluded and can cause sterility

Increase incidence with age

47
Q

What species does endometrial fibrosis occur in?

A

Mare

48
Q

What is endometrial fibrosis in the mare associated with?

A

Trauma

Parturient injuries

49
Q

What is the consequence of endometrial fibrosis?

A

Can result in the mare becoming infertile

50
Q

What species does cystic endometrial hyperplasia occur in?

A

Bitch

51
Q

What occurs in cystic endometrial hyperplasia?

A

Repeated hyperplasia in luteal phase

52
Q

What are the causes of cystic endometrial hyperplasia

A

Bitch not spayed – series of luteal phases, full of cysts

53
Q

What is cystic endometrial hyperplasia assocaited with?

A

Pyometra

54
Q

What management options influence infertility?

A

Oestrus detection - rate and accuracy
Timing of mating/AI in relationship to ovulation
Number of matings (Queen)

55
Q

What are some of the nutritional influences on infertility?

A

Energy / metabolic status
e.g. anovulatory anoestrus, second litter syndrome
Pass energy balance nadir
Reduced gonadotrophin / IGF1 levels (see additional slide)

Vitamin / mineral deficiencies / toxicities: Copper / molybdenum / Selenium
Management of dry / pregnant animal
Oestrogenic substances in plants
Dietary proteins: Increased urea  poor fertility

56
Q

What are pigs/ewes genetic influences on infertility?

A
  • Increased number of ovulation doubled
  • Reduced embryonic survival
  • Uterine capacity
57
Q

What are cows genetic influences on infertility?

A
  • Selection for yield rather than fertility
  • Holsteins: poorer fertility?
  • Heritability for fertility

REPRO2 (31 decks)

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