Exam 3 - Non-infectious Infertility Flashcards

1
Q

what is the most common cause of anestrus/low pregnancy AI rates in cattle?

A

inaccurate estrus detection - occurs 90% of the time, usually no pathology & they are usually in diestrus with a CL

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2
Q

how is non-detected estrus diagnosed?

A

repeated exams - include exams for cows that are ‘in heat’, & make sure you keep accurate records

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3
Q

how can temperature cause anestrus in cattle?

A

very hot or very cold can reduce activity

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4
Q

how can size & location of the yard cause anestrus in cattle?

A

not truly anestrus, but it is too big so the cows never see their friends with benefits

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5
Q

what are some methods in which heat detection is improved for cattle?

A

KaMar paint patches - placed at tail base & splatter when they are mounted

grease pencil thing - cheaper than the paint ones, & it looks like slicked back hair when they are mounted

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6
Q

how do pedometers help with estrus detection in cows?

A

cows in estrus will walk more/show more activity

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7
Q

are teaser animals more commonly used in the dairy cattle or beef cattle industry?

A

more common in beef cattle

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8
Q

what is the most important thing to improve estrus detection in cattle?

A

OBSERVATION

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9
Q

how is PGF2a used to improve estrus detection in cattle?

A

when given, it concentrates the number of cows going into heat at one time when given to a sexually active group of cows (need to have a CL & be in diestrus to respond to this)

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10
Q

what is a gomer bull?

A

bull that has a deviated pp or pp problem that can’t actually breed a cow, but it can be used for detecting cows in estrus

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11
Q

what is a physiologic cause that is often forgotten as a cause of anestrus in cattle?

A

pregnancy!!!

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12
Q

what are the most common pathologic causes of anestrus in cattle?

A

uterine distension from pyometra (persistent CL), mucometra, & hydrometra

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13
Q

why do cows get a pyometra from a retained CL causing anestrus? what cows are often affected by this?

A

they are unable to release PGF2a from their endometrium, so the CL stays & wrecks shop

commonly occurs in postpartum cows

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14
Q

what is the biggest difference between mummified fetuses in cattle & macerated fetuses in cattle?

A

prognosis - mummified fetuses carry a better fertility prognosis

macerated has a poor fertility prognosis

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15
Q

when do mummified fetuses occur in cattle? what pathology is seen?

A

3-8 months into gestation - fluid resorption & sterile environment

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16
Q

when do macerated fetuses occur in cattle? what pathology is seen?

A

any stage of gestation but usually after bone formation!!!!!

vaginal discharge & probably stinky and smelly

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17
Q

which one is macerated & which one is mummified?

A

mummified - top photo, dried up fetus

macerated - bottom picture, infected & gross

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18
Q

T/F: cystic ovarian disease affects 10-30% of dairy cows & is less common in beef cattle (unless they are frequently superovulated)

A

true

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19
Q

what is cystic ovarian disease in cattle?

A

follicle-like structures that fail to ovulate - follicular cysts

or partially lutenized cysts with thicker walls that are usually single - luteal cysts

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20
Q

what are the differences between follicular cysts & luteal cysts in cattle?

A

follicular - > 25mm in diameter, thin-walled

luteal cyst - thicker walled, usually single

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21
Q

what is the mechanism of cystic ovarian disease in cattle?

A

inadequate LH release or lack of LH receptors

stress near calving/hereditary predisposition

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22
Q

T/F: cystic ovarian disease in cattle is more common at or after the 3rd lactation

A

true

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23
Q

what are the clinical signs associated with cystic ovarian disease?

A

70-80% anestrus

20-30% nymphomania - mounting other cows constantly or sterility hump with a prominent tail head

occasional masculinization

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24
Q

this is a sterility hump - what condition is this appearance associated with?

A

cystic ovarian disease

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25
Q

how is cystic ovarian disease diagnosed in cattle?

A

history & clinical signs

palpation/ultrasound

uterus is flaccid!!!!!!!

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26
Q

why is no treatment sometimes used for cystic ovarian disease in cattle?

A

none due to spontaneous recovery - 60% before 1st postpartum ovulation & 20% after 1st postpartum ovulation

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27
Q

what treatment is used for follicular cysts in cattle?

A

GnRH - stimulates LH release from AP, gets them to estrus in 3 weeks

hCG - LH activity, normal cyclicity in 3 weeks with 65-80% responding to a single dose, but if no response to the 3rd treatment, bad news

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28
Q

what treatment is used for luteal cysts in cattle?

A

PGF2a given 9-10 days after GnRH or hCG

estrus in ~3 days, so estrus from treatment takes 12 days instead of 3 weeks

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29
Q

T/F: it is cost effective to exam cows for cystic ovaries 50-60 days postpartum to determine if treatment is needed & then treating what is necessary

A

true

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30
Q

T/F: manual rupture of luteal cysts is an okay treatment option for cystic ovarian disease in cattle

A

false!!! very bad - risk of hemorrhage especially with luteal cysts

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31
Q

how do freemartins happen in cattle?

A

anastomosis of fetal vessels of twin baby cows - male differentiation occurs earlier than female differentiation, so there is a transfer of the H-Y antigen which inhibits female gonadal development

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32
Q

T/F: >90% of twin calves are affected by freemartinism

A

true

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33
Q

what animals are affected by freemartinism?

A

female co-twin of male calf

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34
Q

what are the clinical signs of a freemartin cow?

A

hypoplastic ovaries

hypoplasia/aplasia of the tubular tract (varying degrees) but uterus & vagina usually don’t communicate

35
Q

how are freemartins diagnosed?

A

tube test - take a blood tube & pass it into the vagina, & if it is a free martin, it won’t go in

also ultrasound/palpation/history

36
Q

what is ovarian hypoplasia of cattle?

A

sporadic occurrence (autosomal recessive gene, incomplete penetration) - partial/incomplete but can be unilateral or bilateral

37
Q

what clinical signs are associated with ovarian hypoplasia of cattle?

A

ovaries are bean sized in the broad ligament, but may be near to normal

tubular organs - underdeveloped (can see complete bilateral cases) or may just be slightly affected

38
Q

how is ovarian hypoplasia diagnosed?

A

palpation - hard to identify the ovaries, may not be able to find them during palpation, or just a very very small reproductive tract

39
Q

what is another name for segmental aplasia? why?

A

white heifer disease - happens in white/gray breeds (all breeds with white offspring), common in short horn breeds (recessive in white shorthorns)

40
Q

what is wrong with this reproductive tract?

A

ovarian hypoplasia

41
Q

what is wrong with this reproductive tract?

A

segmental aplasia

42
Q

what clinical signs are associated with segmental aplasia?

A

cranial reproductive tract is normal but caudal horn is aplastic & they accumulate fluid & is commonly confused with pregnancy, can end up being a hydrometra or mucometra

43
Q

what are the greatest affects from underfeeding causing nutritional infertility in cattle?

A

high metabolic demand - puberty, parturition, peak lactation, first calf heifers

delayed puberty

delayed uterine involution

prolonged postpartum anestrus!!!!!!

44
Q

what are the greatest affects from overfeeding causing nutritional infertility in cattle?

A

fat cow syndrome - cows refuse to eat, fatty liver

reproductive disorders - dystocia, retained placenta, metritis

metabolic disorders - displaced abomasum, mastitis, ketosis, & milk fever

fail to respond to treatment!!!

45
Q

in ewes & does, why do you cull all open or ‘poor doers’ annually?

A

they typically have high fertility

46
Q

what is the intersex condition seen in goats?

A

polled gene is an autosomal dominant gene & the intersex (infertility gene) is linked to the polled gene BUT is RECESSIVE

polled buck/doe can be heterozygous or homozygous

if they are polled but fertile, they must be heterozygous!!!

47
Q

how do you prevent intersex from occurring in goats?

A

breed with at least one parent having horns!!!! ensures that none of the offspring will be homozygous for the polled gene & therefore won’t be intersex

48
Q

what does polled mean?

A

no horns

49
Q

what clinical signs are seen in intersex goats?

A

intersexuality in homozygous genetic females (XX) that are male pseudohermaphrodites

infertility in homozygous genetic males

so their gonads are testis that produce a lot of testosterone

enlarged clitoris & young anestrus doe that teases other does

50
Q

why are hydrometras confusing in goats?

A

it is an accumulation of intrauterine fluid that develops after mating that is often confused with pregnancy because it happens around the time you would expect the doe to give birth!

51
Q

what clinical signs are seen in goats with hydrometras?

A

abdominal distension

persistent CL (anestrus)

fluid expelled after 150 days - cloud burst

52
Q

what is the etiology of hydrometras in goats?

A

unsure but we think it is a lack of normal prostaglandin release

53
Q

what is the treatment for hydrometras in goats? what is the prognosis of their return to fertility?

A

give them PGF2a

good

54
Q

what are some clinical signs of ovarian cysts in goats?

A

follicles > 1.2cm, considered cysts!

short interestrus intervals & nymphomania in the middle of the breeding season - erratic estrus (normal at the beginning & end of the season)

55
Q

how are ovarian cysts diagnosed in goats?

A

presumptive diagnosis - confused with poor heat detection

based on history - impossible to palpate their ovaries!

56
Q

how do you treat ovarian cysts in goats?

A

hCG or GnRH - get rid of the cysts & get them back into normal cycles

57
Q

how is the seasonal transition a cause of abnormal cycles in horses?

A

erratic/prolonged activities of receptivity with no ovulation

changes in melatonin causing problems

58
Q

what may cause prolonged diestrus in a horse?

A

retained/persistent CL (stays 30-90 days)

59
Q

what are some causes of prolonged diestrus in horses? how do you treat it?

A

inadequate endometrial prostaglandin release

diestrus ovulation

idiopathic

CLINICALLY VERY IMPORTANT!!

PGF2a

60
Q

T/F: seasonal anestrus accounts for 75-80% of non-infectious infertility in horses

A

true

61
Q

silent estrus is most commonly seen in what horses?

A

mares with foals

maidens

mares with inadequate teasing time

overly aggressive stallion around a mare - freaks her out

62
Q

what is silent estrus?

A

horse is having a normal estrus/ovulation but not showing signs that it is happening

63
Q

how do you treat silent estrus in mares?

A

improve the teasing program

change the stallion

sedation used for them to breed

synchronization

64
Q

what is turner’s syndrome in horses?

A

63 XO karyotype - 63 instead of 64 chromosomes causing gonadal dysgenesis

65
Q

what clinical signs/physical abnormalities does turner’s syndrome cause in mares?

A

anestrus

underdeveloped uterus - endometrial hypoplasia

hypoplastic ovaries - small & inactive

head is disproportionately large

66
Q

what do you thing is wrong with this mare? why?

A

turner’s syndrome - big head

67
Q

why is this going to be a problem for this mare?

A

poor perineal conformation - poop will fall into the vagina & cause vaginitis/cervicitis/endometritis & can get pneumovagina/pneumouterus

68
Q

how do you treat these?

A

caslick’s procedure

69
Q

what is the pathology shown here? what can cause it? what is the sequela of it?

A

urovagina !

trauma or poor conformation

urine pools in the anterior vagina & contaminates the uterus & is spermicidal

70
Q

what is this? what mares are affected by it? what do you do about it?

A

persistent hymen

maiden mares

manually perforate it

71
Q

what is this seen in the vagina of a mare? what can cause it? does it affect fertility? what is a differential you should have for this?

A

varicosities - older mares in late pregnancy, bleeding from the vulva

doesn’t cause infertility

placentitis as a differential

72
Q

what mares are affected by periglandular fibrosis? what is seen on biopsy?

A

older mares - connective tissue is deposited around glands causing nests, cystic gland distension, & inspissations

73
Q

how is periglandular fibrosis diagnosed in horses?

A

endometrial biopsy

74
Q

what is seen on this endometrial biopsy of an older mare? is there any treatment?

A

periglandular fibrosis - no treatment

75
Q

what are the sequela of periglandular fibrosis in a mare?

A

pregnancy lost!!!! big impact with severity & frequency

76
Q

why are endometrial cysts & lymphatic lacunae a problem for equine uteruses?

A

can be confused with early pregnancy & can also interfere with early pregnancy!!!!!

77
Q

how are endometrial cysts & lymphatic lacunae diagnosed in a mare?

A

endometrial biopsy!!!!

78
Q

what horses are commonly affected by endometrial cysts & lymphatic lacunae? why do we think it happens?

A

older mares - inadequate lymphatic drainage!!!

79
Q

what is the most common reproductive neoplasia seen in mares? is it benign or malignant?

A

granulosa-thecal cell tumor!!!!!

usually benign & unilateral

80
Q

what mares are commonly affected by granulosa-thecal cell tumors?

A

prevalence increases with age!!!! still can be seen in younger animals

81
Q

what are the clinical signs associated with granulosa-thecal cell tumors in mares?

A

anestrus, erratic-estrus, stallion-like behavior, & masculinization

tumor produces testosterone!!!!! this is why we see signs

82
Q

what are some differentials for granulosa-thecal cell tumors?

A

cystadenoma, teratomas, dysgerminomas - typically hormonally inactive

hematomas, abscess, anovulatory follicle (will fill up with blood, sterile event)

83
Q

what is felt on the affected ovary with a granulosa-thecal cell tumor? what about the unaffected ovary?

A

loss of the ovulation fossa!!!!!! the affected ovary is enlarged!!!!!

other ovary is small & inactive - hormonal feedback from the tumor may be from testosterone, inhibin, & AMH