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Year 3 repro > cow fertility and repro > Flashcards

cow fertility and repro Flashcards

1
Q

What does a normal follicle look like?

A

transient, soft

1.5 - 2cm in oestrus

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2
Q

What does a vacuolated CL look like?

A

same size as normal CL

vacuole disappears during pregnancy

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3
Q

how does a lutenised follicle appear?

A

over 2.5 cm
large vacuole
from anovulatory mature follicles
occur early postpartum

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4
Q

how does a follicular cyst appear?

A 
thin walled
oestradiol secreting
over 2.5 cm
single / multiple / uni/bi lateral
causes subfertility
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5
Q

how does a luteal cyst appear?

A 
thick walled
over 2.5cm
P4 secreting
single
cause subfertility
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6
Q

how does an inactive cyst appear?

A

thin walled
inactive
single / multiple / uni / bi lateral
result of sub-fertility

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7
Q

What can cause no observed puberty in the heifer?

A
  • ovarian aplasia and hypoplasia

- freemartinism

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8
Q

How do you diagnose a freemartin?

A

test tube - how far does it go in (only 5 cm = +ve)

karyotyping

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9
Q

Causes of no observed oestrus in a cow?

A
  • anoestrus / acyclicity (high yield, low energy, poor BCS, stress)
  • ovarian cysts
  • persistent CL
  • suboestrus
  • failure to detect oestrus
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10
Q

how does poor energy intake cause anoestrus?

A

poor energy intake = low IGF1 with decreases GnRH, embryo growth, ovary steroidgenesis and luteal activity

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11
Q

what is found on a clinical exam with a cow with anoestrus?

A
  • smooth and flat ovaries
  • small follicles, no CL
  • milk p4 stays low
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12
Q

How can you treat anoestrus / acyclicity?

A
  • get back into +ve energy balance
  • improve nutrition
  • GnRH
  • CIDR / PRID
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13
Q

What causes ovarian cysts?

A
  • anovulatory grafiaan follicle where the granulosa cell layer degenerates so the cow become acyclic or nyphomaniacal
  • failure of LH surge
  • few LH receptors in granulosa cells of cysts
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14
Q

How do you treat ovarian cysts?

A
  • dont rupture
  • luteal - PGF2a
  • Follicular GnRH then PGF2a or CIDR / PRID
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15
Q

what is the problem with a persistent cL?

A

pyometra interferes with leutolysis

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16
Q

How do you treat a persistent CL?

A

PGF2a

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17
Q

What can cause suboestrus?

A

non cow friendly environment

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18
Q

What are the signs of oestrus?

A 
restless
not eating
low milk
searching for other cows
mounting / standing
group
bellowing
clear vulval elastic mucus discharge
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19
Q

What are the causes of failure to detect oestrus?

A
  • cow oestrus

- person problem

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20
Q

How could you overcome poor oestrus detection?

A
  • put a bull in
  • ovsynch
  • synchronise herd
  • heat mount detectors
  • measure milk p4
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21
Q

What can cause return to oestrus after service?

A
  • not calving
  • anovulation
  • delayed ovulation
  • incorrect AI timing
  • hormonal imbalance
  • structural defects
  • infection
  • nutritional imbalance
  • stress
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22
Q

cow embryopathic organisms

A 
campylobacter fetus
tritrichomonas fetus
mycoplasma
BVDV
IBR
chlamydia
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23
Q

what is a regular return to oestrus?

A

return to oestrus 18-24 d after AI

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24
Q

what is an irregular return

A

return to oestrus 24 d

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25
Q

what does it mean if sum of 2 consecutive returns is about 42 d?

A

AI timing incorrect

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26
Q

what is a cow a repeat breeder?

A

returned on 3/4 consecutive occasions

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27
Q

what does abnormal vulval discharge indicate?

A

endometritis / metritis

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28
Q

what are causes of endometritis / metritis?

A 
-long or short gestation
retain membranes
parity
yield
dystocia and trauma
hygiene
nutrition
repeat breeder
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29
Q

how do you treat endometritis?

A
  • CL present = PGF2a
  • no CL = intrauterine cephalosporin
  • chronic = peridine iodine
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30
Q

how is an abortion classified?

A

<271 d dead / alive for less than 24 hr

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31
Q

non infectious causes of abortion and stillbirth

A 
genetic
endocrine
toxins
heat stress
iatrogenic
dystocia
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32
Q

infectious causes of abortion and stillbirth

A 
truperella pyogenes
leptospira
bacillus
BVDV
neospora
e.coli
strep
fungi
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33
Q

what is the voluntary waiting period? what can extend it?

A
  • management decision for earliest service date (when she starts cycling)
  • extended by dystocia, metabolic problems, disease
  • normally 42 d
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34
Q

what is the calving - 1st service interval? and what affects it?

A
  • normally 65 d (ESD +21)

- affected by VWP , postpartum problems, return to cyclicity, poor oestrus detection

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35
Q

what is the first service submission rate?

A

proportion of cows served within 3 weeks of ESD, aim ~ 85 %

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36
Q

why do we measure first service submission rate instead of calving - s1?

A
  • calving to s1 is affected by cows not served, unusual VWP and any late / early cows cancel out
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37
Q

what is the aim for calving to conception interval?

A

85 d

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38
Q

what is the aim for the calving interval?

A

365 d

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39
Q

what will milk p4 be during oestrus

A

<5ng/ml

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40
Q

how can we look at how well conception is on a graphical form?

A

q/cu - sum graph

  • move one box up if conceived and one down if didnt
  • plot on x axis calf number and date of AI
  • can see what hapenned on what days
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41
Q

what animals would you examine on a routine visit?

A
  • problem animals
  • post calving / pre breeding
  • irregular returns
  • oestrus not observed
  • PD
  • pregnant
  • odd events
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42
Q

What is a good conception rate?

A

~ 60%

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43
Q

if see bulling which cow do you AI now?

A
  • cow on bottom

- cow on top keep an eye on as coming into heat soon

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44
Q

how many joules is one calorie?

A

4.2 j

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45
Q

how many mJ / L of milk?

A

5mj/l of milk

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46
Q

how much extra energy do high activity cows need?

A

19mj / day

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47
Q

how much extra energy is needed for the first 2 months of pregnancy?

A

0.5 m j /day

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48
Q

how much extra energy is needed for month 4 of pregnancy?

A

1.6 mj / day

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49
Q

how much extra energy is needed for month 6 of pregnancy?

A

5.0 mj / day

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50
Q

how much extra energy is needed at full term ?

A

35 mj/day

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51
Q

how much extra energy is needed for an overdue calf?

A

44 mj / day

52
Q

how much energy is mobilised by 1 kg weight loss?

A

35 mj

53
Q

what 2 factors decrease voluntary feed intake?

A

around calving

fat cows

54
Q

what are high protein sources of food?

A

protein meal
fishmeal
NPN

55
Q

what are moderate protein sources?

A

alfalfa

legume

56
Q

what are low protein sources?

A

grass hay
cereals
straw

57
Q

when is pregnancy toxaemia most commonly seen in cattle?

A

thin, twin, beef cattle

58
Q

how can you prevent pregnancy toxaemia?

A

dry off at BCS 3 and calve at 3

59
Q

what is normal fat metabolism around calving?

A

around calving get a normal mobilisation of fat so increase FA in blood is normally dealt with by the lvier

60
Q

what causes fatty liver disease?

A 
fat dry cow
dry cow on a diet
fat cow at calving not eating
dry cow having sudden diet change
excessive weight loss post partum
61
Q

what can be the consequences of fatty liver disease?

A 
immunosuppression
retained foetal membranes
endometritis
infertility
ketosis
mastitis
62
Q

what are the 9 ways to PD?

A

1) non return to oestrus
2) ultrasound from 30 d transrectal
3) milk and plasma p4
4) membrane slip from 35 d
5) disparity in horn size from 35 d
6) plapation of foetus 45-60 d
7) presence of placentomes from 80d
8) fremitus of middle uterine artery from 85 d
9) oestrone sulphate in milk and plasma from 105 d

63
Q

how can milk and plasma p4 predict pregnancy?

A

during oestrus p4 should drop
if it doesnt then pregnant of luteinised cyst or persistent CL, incorrect AI timing
if low then def not preg

64
Q

what can cause a false positive in horn size disparity?

A

incomplete involution
fluid
pus mucous

65
Q

what is fremitus in the uterine artery?

A

hypertrophy of the artery (middle uterine artery) in the broad ligament
can feel increased turbulence of blood flow

66
Q

what can oestrone sulphate tell you?

A

only present after d 105 if there is a live foetus

produced by foeto-placental unit and conjugated to sulphage

67
Q

What is the difference in early and late embryonic mortality?

A

early is before maternal recognition and late is after

early you get a regular return to oestrus, late you get an irregular return

68
Q

what day does embryonic loss become foetal loss?

A

d 42

69
Q

How can BCS affect pregnancy rate?

A

if low 5w post partum then get lower conception rates

70
Q

what are 4 common pregnancy complications?

A

1) hydrops
2) uterine torsion
3) cervical vaginal prolapse
4) uterine prolapse

71
Q

what are the two types of hydrops that can cause pregnancy complications?

A
  • placental oedema

- foetus

72
Q

what can you do with a cow with placental hydrops?

A
  • normally in last 3 m
  • cull
  • induce parturition
  • drain fluid and C section
73
Q

what are the types of foetal hydrops and what can you do?

A
  • hydrocephalus, ascites, anasarca (inside out)

- fetotomy, C section

74
Q

How do you diagnose and what can you do about uterine torsion?

A

diagnose by vaginal and rectal exam

reposition internally or externally

75
Q

what can predispose to cervical / vaginal prolapse?

A
  • high / low BCS
  • high roughage diet
  • twins
  • high oestrogens
  • lack of exercise
  • urinary retention
  • breed
  • age
76
Q

what can be the consequences of cervical vaginal prolapse?

A

infection
inappetance
urinary retention
rupture and guts out

77
Q

what can you do to treat a cervical vaginal prolapse?

A

analgesia
epidural
spoon / harness
sutures shut

78
Q

what do you do with a uterine prolapse?

A 
remove foetal memebranes
epidural block
put in frog position
keep pushing (all the way in, use a bottle)
calcium borogluconate
relieve ruminal tympany
79
Q

what is eutocia?

A

normal parturition

80
Q

what is prodrome?

A 
stage 1 labour
foetal positioning
cervix dilation
foetal membranes exposed
behaviour
81
Q

what is puerperium?

A

recovery of genital tract post partum

82
Q

what are the 2 categories of maternal dystocia cuases?

A

expulsion

birth canal

83
Q

what is the category of foetal dystocia causes?

A

disposition

84
Q

what are the maternal expulsion causes of dystocia?

A

uterine inertia

defective / inadequate straining

85
Q

what are the maternal birth canal causes of dystocia?

A

failure of cervix, soft tissues or ligaments to relax

uterine torsion

86
Q

what are the maternal and foetal components of foetal maternal disproportion?

A

maternal - inadequate pelvic diameter

foetal - too large

87
Q

what are the foetal disposition causes of dystocia?

A

abnormal presentation
position
posture

88
Q

if calf presenting normally and carpal joint is 10 cm out how much force is needed?

A

2 people pulling

89
Q

if double muscled calf how much force is needed

A

1 person pulling only

90
Q

what do you do once the head is out to get the hips to fit?

A

rotate 90 degress and pull dorsally so hips fit

91
Q

what are the 3 aids

A

chains
head snare
hooks in eyes

92
Q

if presenting caudally and hock is 10 cm out how much force is needed?

A

2 people pulling

93
Q

which way do you pull a normal vs caudal presenting calf?

A

normal - pull downwards

caudal- pull dorsally

94
Q

what is foetal presentation? and what are the 3 types

A

relationship between longitudinal axis of dam and baby

longitudinal anterior
longitudinal posterior
transverse

95
Q

what is foetal position and what are the 3 types?

A

relationship between dorsal foetus and top of canal

dorsal
ventral
lateral

96
Q

what is foetal postures and what are the 3 types?

A

disposition of foetal appendages

limb flexions
neck flexions
head displacements

97
Q

what is the normal postures, presentation and position of a calf?

A

normal posture, dorsal position, longitudinal anterior presentation

98
Q

what are some causes for foetal disposition?

A 
weak uterine contraction
oversized calf
delayed development of foetal reflexes
weak foetal movements
competition for uterine space
ankylosis of joints
99
Q

What is the normal process of involution?

A

shift from hypertrophy to atrophy
reduction in size of myofibrils
influenced by prostaglandins and oxytocin

100
Q

What happens to the uterus during involution?

A

greatest decreased in first few days
by 8-10d uterus should all be palpable per rectum
normal by 26-50 d

101
Q

what happens to the cervix during involution

A

after 96 h only 2 fingers can fit
normally at 25d the diameter of the cervix should exceed that of the previously gravid horn
back to normal in 60 d

102
Q

how does the endometrium regenerate post partum?

A
  • Caruncles - degenerate, become necrotic as ischaemic and slough off
  • Lochial discharge - sloughed necrotic material, blood, foetal fluids, for 2-9 d pp, yellow/reddish brown, no odour, 0.5 - 2l
103
Q

How are contaminants eliminated post partum?

A

phagocytosis by migrating leucocytes, physical expulsion by uterine contractions and secretions

sterile within 8-9 w

104
Q

How does cyclical activity resume post partum?

A
  • during pregnancy P4 feeds back on the pituitary so it becomes regractory to GnRH pp
  • after 7-10 d get FSH surge and a follicular wave in the opposite horn to the pregnancy and will only ovulate if follicle makes enough oestradiol
  • often gets a shorter luteal due to poor follicle development so an inadequate CL
  • this is delayed by suckling
105
Q

what are 4 factors that can disrupt any events of the puerperium?

A

dystocia / Caesar
uterine prolapse
retained foetal membranes
uterine disease

106
Q

what are the 4 normal processes in puerperium?

A

involution
regeneration of the endometrium
elimination of contaminants
resumption of ovarian cyclical activity

107
Q

How can dystocia / caesar disrupt puerperium events?

A
  • break host defences
  • physical deformity and tissue damage to vulva and cervix so more prone to contaminants
  • uterine inertia so cant expel contaminants
108
Q

how can a uterine prolapse disrupt puerperium events?

A

can increase conception times

109
Q

why does a uterus prolapse?

A

straining in stage 3
flaccid uterus
gravity

110
Q

what are the risk factors fro a uterine prolapse?

A

pluriparous
increased parturition time
compromised tone
increased abdominal straining

111
Q

why do retained foetal memebranes affect puerperium events?

A

predispose to uterin inf and infertility

112
Q

why do you get retained foetal memebranes?

A

failure of placental maturation
failure of detachment
inadequate uterine contraction

113
Q

how do you treat retained foetal membranes

A

wait 5 d for a vet
can try gentle traction
dont use abx as want it to putrefy
collagenases in umbilical a

114
Q

what are the risk factors for retained foetal membranes?

A 
dystocia
premature
abortion
stillbirth
multiples
infectious placentitis
hypocalcaemia
hydrallantois
old
prolonged gestation
micronutritent deficiences
115
Q

How does the placenta normally mature and detach?

A
  • changes in P4 and E2 conc
  • changes in collagenases and proteases
  • change in number of binucleate cells in trophoectoderm
  • distortion of placentomes
116
Q

what are the risk factors for uterine disease pp?

A

dystocia
RFM
high pathogen load
acyclic (as e2 nd p4 needed for local immune system)

117
Q

what are the signs and how do you treat endometritis?

A

signs - mucopurulent discharge, systemically find, neutrophils in uterine luminal fluid, poorly involuted uterus

treat - stimulate oestrus ( cyclic - PGF2a, non - GnRH), intrauterine cephairin

118
Q

what are the signs and how do you treat metritis?

A

signs - systemically ill, dull, low yield, low appetite, toxaemia, purulent fetid fluid, distended atonic uterus, sore swollena dn inflamed vagina and vulva

treat - stabilise, Abx bacteriocidal as have endotoxaemia, uterine lavage and oxyteracycline

119
Q

what are the signs and treatment for pyometra?

A

signs - acyclic, purulent material, persistent CL, large and distended horns with a closed cervix

treat - PGF2a and intrauterine cephapirin

120
Q

what are the signs of free martinism?

A 
blind ending vagina
no apparant cervix
streaky structures where the ovary is normally
acyclic
no sings of heat
oestradiol very low
progesterone low
no effect from hCG or eCG
prominent clitoris
121
Q

how can you detect the y chromosome in free martins?

A
  • PCR with probes for y-chromosome specific segments
122
Q

how do we get free martins?

A
  • xx and xy twins
  • share blood supply so female exposed to male hormones
  • they have testosterone so the wolfian duct differentiates
  • mullerian ducts dont form properly so blind ending vagina
123
Q

what can you use free martins for?

A

beef
research
oestrus detection

124
Q

how does normal XY develop?

A

1) SRY (sex determining region of Y) signals to testis formation
2) testis make testosterone
3) testosterone acts on mesonephric duct to form male internal genitalia
4) testosterone converted to 5-dihydrotestosterone by genital tubercle and 5 alpha reductase - acts on genital tubercle to make glans penis and scrotum
5) AMH from the testis acts on the mullerian duct so they dont differentiate

125
Q

how is XX development different from XY?

A

1) no SRY so no testis form so get ovaries
2) dont need anything from gonads
3) no androgen from ovaries so not differentiation of wollfian duct
4) no AMH so paramesonephric duct (mullerian duct) becomes the uterus, oviduct and cranial vagina)

Year 3 repro (12 decks)

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