Principle Causes of Infertility in the FEMALE Flashcards

1
Q

Name some of the main causes of infertility in the female?

A
  • Ovaries with some form of pathology
  • Poor or mismanagement
  • NEB
  • Inappropriate timing
  • To get appropriate timing need to be able to detect oestrus – easier in some species than others!
  • Horses ovulate before the end of oestrus – when trying to manage this, it becomes a lot harder, not so much of a problem in the wild
  • Infections of the reproductive tract, mainly uterus – possibly vagina or cervix. Unlikely for the ovary to be infected!
  • Whites in dairy cow
  • Uterus should be aseptic environment! If its not, embryo is unlikely to be able to attach

BOB ROBS LIST:

  1. Aberrant development of the genitalia and/or ovaries
  2. Irregular or abnormal oestrous cycles

•Cystic ovaries comes under here

3.Vulvar or vaginal discharge

•Probably come from endometrium

  1. Failure to become pregnant
  2. Embryonic death
  3. Miscellaneous
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2
Q

Name some of the congenital and developmental anomalies?

A

Largely structural

Animal is largely born with these

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

What is ovarian hypoplasia?

What is the treatment and how common is it?

A
  • One or both ovaries absent (rare)
  • Rare for both ovaries to be absent!
  • Ovarian hypoplasia (uncommon in most species)
  • Virtually no follicles, no cycle, no oestrus
  • Often bilateral
  • Flaccid uterus
  • No treatment
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4
Q

What is segmental dysplasia?

A

Segmental dysplasia of paramesonephric ducts (1 in 1000)

  • Developmental obstruction
  • Ovaries function normally

e.g. Uterine didelphys, Uterine unicornis, Partial aplasia

  • Can establish pregnancy normal etc. – depends on which degree the obstruction is occurring
  • If one horn bigger than horn – can be confused with pregnancy
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5
Q

What is Uterine didelphys?

A

A reproductive tract dysplasia

Uterus didelphys (sometimes also uterus didelphis) represents a uterine malformation where the uterusis present as a paired organ when the embryogenetic fusion of the Müllerian ducts fails to occur. As a result, there is a double uterus with two separate cervices, and rarely a double vagina as well

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6
Q

What is Uterine unicornis?

A

A reproductive tract dysplasia

Uterus unicornis is defined as complete agenesis of one uterine horn. … Ipsilateral renal agenesis is present in approximately 29% of cats with uterineabnormalities

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7
Q

What is seen with a persistence of hymen?

A

•Bulge from vulva

Strain at service (pain to mate

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8
Q

What is this?

A

Uterine didelphys

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9
Q

What is free-martinism?

A

Vascular anastomosis of adjacent chorioallantoic sacs of heterozygous foetuses. Transfer hormones from one animal to other. Female will be masculinised.

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10
Q

What is seen with the repro tract with free martinism?(3)

A
  • Prominent clitoris hairy vulva
  • Paramesonephric ducts absent or grossly hypoplastic
  • Ovaries vestigial and/or masculinarised
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11
Q

How can you diagnose free martinism? (2)

A
  • Failure to detect cervix via a probe or by rectum
  • Sex chromosome chimerism
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12
Q

How many animals who are heterosexual twins turn out to be free martins?

Which animals does it affect (2)?

A

95%

Cows and goats

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13
Q

How can an animal be inter-sex and default to develop female?

A
  • SRY gene on the Y chromosome (it is not activated and therefore they become female)
  • Often female at birth
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14
Q

What are the 3 causes of ambiguous genitalia?

A
  • Spectrum of gonadal types
  • XX: male pseudohermaphrodite
  • XO: Turners syndrome
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15
Q

How can you dianose inter sex?

A

Karotyping

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16
Q

Where is inter sex quite common? (3)

A

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

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17
Q

What is the normal ovary structure?

A

Follicle which houses the oocyte

Follicle grows. Takes many months from primordial to ovulatory

Antral follicles which are seen on U/S- follicular waves form these

Cohort of follicles grow (top U/S pic)- some grow and some undergo atresia. Then get a dominant follicle

You can get a CL and dominant follicle at the same time (see 2nd down U/S pick).

Dominant – dominant over other follicles

Follicular waves happen even with CL

CL produces progesterone

CL prevents D follicle being ovulated

If there is a D follicle and you give GnRH – D follicle will ovulate and form an accessory CL. No chance of being fertilised as in a high progesterone environment (CL)

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18
Q

What can be seen in this pic?

A
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19
Q

What are the 3 most common presentations on a dairy farm for ovarian infertility? (3)

A
  • Persistent CL
  • Not seen bulling – oestrus not observed
  • Silent oestrus
  • Might be in anoestrus – anovulatory and oestrus. Not cycling normal
  • No dominant follicles
  • No CL
  • Very small – hard on rectal
  • Cyst – a large follicle that has failed to ovulate.
  • Often not due to infection – ovulitis is RARE
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20
Q

What can cause a lack/cessation of cyclicity? (2)

A
  • Delayed post-partum or season
  • Associated with NEB
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21
Q

What is the incidence of anovulatory anoestrus? (4)

A
  • Common in dairy cows (especially high yielding)
  • Prolonged anoestrus in bitches
  • Whelped/pseudopregnancy – 200 days (5-7 months). So longer than this
  • Sows (associated with MMA)
  • Pregnancy failure in mare
  • 35 days – form endometrial cups which produce ECG. In essence if they form these and loose pregnancy we cant do much- effectively anoestrus
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22
Q

What is the clinical presentation of anovulatory anoestrus?

A
  • Small, inactive ovaries
  • i.e. no dominant follicle or CL
  • Irregular progesterone profile
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23
Q

What are the pre disposing factors for anovulatory anoestrus? (8)

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

Endometritis

24
Q

What are the 2 underlying encorinolgies of an ovulatory anoestrus?

A

Aberrant LH (and FSH) pulsatile secretion

  • Influenced by negative energy balance
  • Stress (corticosterone)
  • Low stimulation of antral follicular development

Low insulin / insulin-like growth factor 1 (IGF1) levels

  • Directly influence follicular growth and steroidogenesis
  • Low insulin in farm animal – (oftren low in NEG) – follicle growth will be less
25
Q

What is the function of FSH?

A

recruit cohort of antral follicles and increase oestradiol production

26
Q

What is the function of LH?

A

– to allow the follicle to become dominant, stimulate ovulation

27
Q

How can we treat anovulatory anoesturs? (5)

A
  • Eliminate pre disposing factor
  • Hormones:
    • Progesterone – withdraw and it will fall which may help to stimulate them into a follciluar phase. Can use a combo

Gonadotropin based

Combination

Prolactin inhibitors (bitch)

28
Q

What is Cystic ovarian disease?

A

Follicular structures that have failed to ovulate

•Persistent, large follicle(s)

29
Q

What is this?

A

Cystic ovarian disease

30
Q

What is the difference beterrn follicular and luteal Cystic ovarian disease?

A

1.Follicular

  • Thin walled
  • Oestrogen –> nymphomania
  • Typically be in oestrus for longer than expected
  • Dairy cow normal oestrus is 18 hours

2.Luteal

  • Follicle has had some LH - Partial luteinised; thickened wall
  • No ovulised
  • Anoestrus
31
Q

What is the pathogenesis of Cystic ovarian disease?

A

Hormonal insufficiency of LH

Surge centre or anterior PG = not enough GnRH or LH

May not grow enough so not enough oestradiol for +ve feedback to stimulate LH surge

Either way – follicle wont ovulate and will continue to grow

32
Q

How can we diagnose Cystic ovarian disease (3)

A

Ultrasound

  • Differential based on thickness of wall
  • Always check both ovaries
  • Can have big follicle cysts and then the other ovary may have a CL. So can conclude the animal is cycling by the presence of a CL
  • ‘Normal’ CL can have thin walls

Plasma / milk progesterone if you think it is a luteal cyst

•e.g. > 2 ng/ml: indicate luteal tissue

Accurate diagnosis is difficult (dynamic structures) – cannot do it on a one off visit!! IT is a persistent structure you don’t know is persistent until you check again

33
Q

What are the pre disposing factors for Cystic ovarian disease? (4)

A
  • Immediate post-partum period
  • Severe negative energy balance
  • Nutrition e.g. Excessive dietary protein
  • Early weaning in pigs
  • Stress
  • Concurrent disease
  • Ketosis, uterine infections, mastitis
  • Breed (e.g. common in Holstein; rare in beef breeds)
34
Q

How can you treat Cystic ovarian disease? (4)

A

Spontaneous recover -

Hormonal (single or combination)

  • GnRH / hCG (follicular)
  • Cause the follicle to lutenise! And can then get rid of luteal structure with PG
  • Progesterone (follicular)
  • Prostaglandin (luteal)
35
Q

What happens with a prolonged CL?

A

Failure to return to oestrus

CL persists in absence of pregnancy

  • Can occur in (un)mated animals
  • Early post-partum period
  • Secondary endometrial problems
36
Q

What is the cause of a Prolonged corpus luteum? (2)

A
  • Failure to produce endogenous PG
  • Dioestrus ovulation (mare)
37
Q

How common in a prolonged CL?

Cow vs mare

A

mare - 20%

cow - 2%

38
Q

How do you treat a prolonged CL?

A

•Prostaglandin F2a

39
Q

What ovarian neoplasia is there?

A

Stromal tumours

  • Granulosa cell tumour
  • Uncommon (mare, cow, bitch, cat)

Cystadenoma and cystadenocarcinoma – more aggressive In nature

  • Surface epithelium tumours of ovary
  • In women, 90% of ovarian cancer
40
Q

What is this and what is seen with it?

Prognosis?

A

Granulosa cell tumour

Very large, lobulated, some cyst formation (fluid filled).

  • Production of oestrogens / androgen
  • Generally benign with infrequent metastasis
  • Contra-lateral ovary often small
  • Enlarged ovary with multiocular ultrasonographic appearance
  • Elevated plasma testosterone / inhibin due to granulosa cells
  • Can monitor this way

Survival removal with good prognosis

41
Q

Name venereal pathogens causing infertility. (3)

A
  • Bovine venereal campylobacterosis
  • Infectious pustular vulvovaginitis (IPV/IBR)

Contagious equine metritis

42
Q

What is the effect of a systemic infection on fertility?

A

Unlikely to conceive - pyrexic!

43
Q

When is Metritis, endometritis and pyometra seen?

A
  • Post-partum period (associated with retained fetal membranes)
  • Post-mating (mares)
  • Anatomic barrier integrity
  • Cervix closed and high progesterone – perfect environment for infection
  • Following dioestrus
44
Q

How can we treat Metritis, endometritis and pyometra? (3)

A
  • Broad spectrum Abs – effectiveness is debated
  • Lavage
  • Prostaglandin/oxytocin – contraction to expel
45
Q

Managed to detect oestrus and mated appropriately but often pregnancy fails to establish?

What could the reasons be for this? (3)

A
  • Management
  • Inadequate progesterone causes small embryo development
  • Embryo needs to release maternal recognition of pregnancy factors
46
Q

What can cause fertilisation failure? (3)

A
  • Inappropriate timing of AI/mating
  • Delayed ovulation = aged oocyte
  • Chromosomal abnormalities
47
Q

What can cause early embryo mortality? (3)

A
  • Poor embryonic development
  • Failure to secrete maternal recognition signal
  • Aetiology unknown
  • Lack of progesterone
  • Attenuated uterine / oviductal secretions of histotroph
48
Q

What are the acquired repro tract adhesions? (3)

A

Adhesions (e.g. Ovario-bursal, hydrosalphinx)

  • Increase incidence with age
  • Lumen occluded and can cause sterility

Endometrial fibrosis (mare)

  • Trauma = fibrosis
  • Associated with parturient injuries
  • May become infertile – embryo cant attach to endometrium

Cystic endometrial hyperplasia (bitch)

  • Repeated hyperplasia in luteal phase
  • Not spayed and not pregnant – phases of luteal and develop endometrial hyperplasia.
49
Q

What repro tract neoplasia do we get?

A

e.g. Uterine, cervical vaginal/vulval tumours

  • Uncommon/rare
  • Might not be associated with infertility
50
Q

What can we do management wise to help infertility? (3)

A

Oestrus detection

  • Rate and accuracy
  • If we don’t detect how can we manage. About 50% in dairy!

Timing of mating / AI in relationship to ovulation

Bitch important! When they ovulate huge change in discharge

Number of matings (queen)

  • Commonest cause of “infertility”
  • Induced ovularer – need to release eggs. Single mating may not be enough
51
Q

What are the nutritional inclfuences on infertility? (4)

A
  • Vitamin / mineral deficiencies / toxicities
  • Copper / molybdenum / Selenium
  • Management of dry / pregnant animal
  • Oestrogenic substances in plants
  • Dietary proteins
  • Increased urea
52
Q

How can we manage expectations with infertility? (5)

A
  • Ram:ewe ratio
  • Early induction of oestrus (season; transition period)
  • Lactation and time of weaning (sows)
  • Wean sows earlier - return to oestrus later?
  • Lower fertility at foal heat
  • Voluntary waiting period (cows)
53
Q

What can affect fertility with piges/ewes? (3)

A
  • Increased number of ovulation doubled (ovulate more than one at once)
  • Reduced embryonic survival – limited uterine capacity
  • Uterine capacity
54
Q

What can affect fertility in cows? (3)

A
  • Selection for yield rather than fertility
  • Holsteins: poorer fertility?
  • Heritability for fertility
55
Q

What can cause functional sub/infertility? (4)

A
  • Anoestrus
  • Pathological ovary
  • Conception and early embryo mortality
  • Ovarian inadequacy
  • Reproductive tract lesions
  • Trauma, neoplasia
  • Infectious
  • Loss of pregnancy
  • ‘Perceived’
56
Q

What venereal pathogens affect horses? (4) What are the effects?

A
  • Granular vaginitis (‘nodular venereal disease’) in cattle:
  • Papular eruptions on the vulva mucosa
  • Ulceration, lymphoid follicles
  • Bovine venereal campylobacterosis
  • Vaginitis / endometritis
  • Infertility
  • Infectious Pustular Vulvovaginitis (IPV/IBR)
  • highly contagious herpes infection
  • Spread by coitus and close contact
  • hyperaemia of vulval and vaginal mucosa
  • a mucopurulent discharge
  • Limited affect on fertility
  • Contagious equine metritis
  • Taylorella equigenitalis
  • Embryonic loss