Week 3 Flashcards

1
Q

describe the hormonal changes in parturition of the cow in pregnancy?

A

late pregnancy - oestradiol rises gradually to reach peak

progesterone begins to decline + drops before parturition (CLs still produce progesterone)

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2
Q

describe the hormonal changes in sheep during parturition?

A

progesterone rises considerably from mid=pregnancy

oestrdial remains low until peak before parturition.

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3
Q

describe the hormonal changes in mare during parturition?

A

oestragrens reach peak in mid-pregnancy while progesterone declines
CLs progesterone conc declines dramatically

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4
Q

what else occurs in mare during partursition with cortisol and myometrial activity?

A

a rise in cortisol occurs during days of parturition

Myometrial activity increase at night in peripoant mare, thus mares feed predominantly at night

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5
Q

why must progesterone decline for parturition?

A

reduces functions to occur - increased oestrdiol
decreased progesterone
leads to onset of labour

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6
Q

describe how the fetal hypothalamus has a effect on fetal cortisol levels rising?

A

fetal hypothalamus release CRF
fetal Ant. Pititaru release ACTH
Feta; adrenal glands release cortisol levels that rise and travel to placenta.

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7
Q

describe how sheep fetal cortisol crosses the mature placenta and causes oestradiol synthesis?

A

cortisol diffuses across mature placenta membrane via PGE2 - 17a hydrolase aromatase which causes pregnenolone to covert into oestrdiaol synthesis.

oestradiol induces contractility active proteins in the myometrium, such as PGF2a and oxytocin receptors

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8
Q

describe how cow fetal cortisol induces PGF2a and causes luteolysis?

A

fetal cortisol crosses membrane increases levels of oestradiol and PGF2a causes CL regression in ovary leading to lowered progesterone levels.

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9
Q

what else does PGF2a cause in parturition?

A

uterine contractions, cervical dilation and aids fetal expulsion via relaxin release and oxytocin responsiveness.
relaxin levels increase in mare/bitch.

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10
Q

how does cortisol achieve the increase in oestriaol and decline in progesterone which is essential for parturition?
in placenta?

A

placenta responsible for progesterone production at the end of pregnancy - fetal cortisol induces 17a Hydroxylase + aromatase in the placenta
leads to C21 steroids used as a precursor for oestrdiaol production
oestradiol rises and progetsone falls.

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11
Q

how does cortisol achieve the increase in oestriaol and decline in progesterone which is essential for parturition?
in CLs?

A

corpus luteum (or CLs) is responsible for progesterone production at the end of pregnancy
Fetal cortisol induces placental PGF2a synthesis -
Luteolysis of the CL -
Acute prepartal progesterone decline -
Placental oestradiol synthesis is increasing

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12
Q

describe labour stage 1?

A

preparation - fetus changes position in uterus + enters birth canal
mother becomes restless, vomiting, sweating
mammary gland changes - oedema in mammary gland
- dripping colostrum
- expulsion of cervial plug

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13
Q

describe labour stage 2?

A

expulsion of foetuses (mins)
abdominal contractions viable - foetus delivered though birth canal in the aminon.
escape of allantoic fluid, strong uterine contractions. amino may rupture

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14
Q

explain the Ferguson + Pudendal reflex?

A

1) vaginal = cervical stretching leads to oxytocin release causing smooth muscle contractions
2) N.pudendus reflexes: vaginal stretching leads to strong abdominal contractions

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15
Q

describe labour stage 3?

A

placenta expulsion of first ducklings/standing up
after birth delivered.
repute of umbilical cord
expulsion of fetal membrane 1-12 hours post partum
beginning of puerperium (post partum blood)

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16
Q

name the basic neonate adaptations?

A
cortisol rise 
thyroid T3 hormone rise 
Cord Clamping 
Cold shock 
neonate breathing 
fetal lung fluid secretion 
thermoregulation (non-shivering thermogenesis)
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17
Q

explain the cortisol rise before birth and what its functions for?

A

lung anatomical devopelment, maturation + sue faction synthesis
clearance of fetal lung fluid
matyrationof thyroid axis + more conversions of T4 - T3 leading to rise in thyroid hormone

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18
Q

what does increasing thyroid hormone T3 do afterbirth?

A

stimulates thermogenesis

regulates maturation of the repsiratory, nervous system

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19
Q

discuss what cord clamping is?

A

leads to catecholamine surge within minutes of delivery
the NA + A surge is a response to hypoxia leads to = large increase in B.P
thermogenesis from brown adipose tissue (lipolysis = heat)
these hormones place neonate into ‘Catabolic state’
glycolysis + lipolysis occur which elevate glucose + free FA depleted by 2-3hours
insulin rises after colostrum feed intake to ensure nutrient uptake

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20
Q

explain the stages of neonate breathing?

A

1) cleansing of fetel lung fluid - reversal of fluid secretion + reabsodprption
Areation of the alveoli + INNITAION OF O2 + CO2 exchange between pulmonary capillary blood + gas.
2) surfactant secretion - new alveolar lining layer on liquid hypophase
3) continuous breathing pattern devoplment ex-utero when umbilical cord is calmed to hypoxia leading and cold stimuli

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21
Q

describe fetel lung fluid secretion?

A

1) high secretion in late gestation
2) decline in airspace fluid volume during birth
3) sodium pump responsible for reabsorption of lung fluid into blood vessels + lymphatics

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22
Q

what occurs when new-born takes first breath?

A

air enters bronchi - alveoli move fluid into distal airspace where it is absorbed, O2 can now move in

alveolar fluid is absorbed through the intertsiutm.
O2 transports form alveoli to blood vessels - increasing pO2

in 3 breaths = 50% of the lungs become aerated.

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23
Q

what must happen when neonate lungs are breathing?

A

neonate lungs must allow gas exchange by surfactant production + function.
surfactant reduces inflation resistance + ensures alveoli do not collapse after expiration.

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24
Q

what considerations occur when the fetal circulation oxygen and flow occur?

A

left shift - causes loads of O2 to low O2 tension
High pulmonary vascular resistance in fetal lungs due to low oxygen tension
umbilical vein O2 saturation is 80% with some flow bypassing liver enters caudal vena cava via DUCTUS VENOSUS

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25
Q

what is the ductus Venous?

A

shunts a portion of umbilical vein blood flow directly to the inferior vena cava. allows oxygenated blood from placenta to bypass the liver

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26
Q

where does the caudal vena cava flow direct too?

A

to right atrium + foramen ovale to left atrium P ventricle pumped into aorta.

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27
Q

what is the foramen ovale?

A

small hole located in the septum, which is the wall between the two upper chambers of the heart (atria). Before a baby is born, it does not use its lungs to get blood rich in oxygen.

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28
Q

what is the ductus arteiosus?

A

blood vessel that connects the pulmonary artery (main vessel supplying the blood to the lungs) to the aorta This connection is present in all babies in the womb, but should close shortly after birth.

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29
Q

what does the ductus arteiosus join too?

A

joins aorta downstream of arteries to heal and fix - aortic blood O2 saturation is reduced to 58%

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30
Q

what controls the transition of fetal circulation to adult circulation?

A

cortisol + catecholamines - leads to increased lung perfusion + O2 pressure.

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31
Q

what changes occur from transition of fetal circulation to adult circulation?

A

2x cardiac output with rise in O2 consumption due to increased metabolism, breathing effort, thermogenesis.
increased B.P
blood flow - lungs, heart, kidneys, GIT etc

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32
Q

what do the changes in B.P causes in the atria + aorta + pulmonary artery?

A

cause closure of foramen ovale + ductus arteriousus = aortic pressure causes back flow through PA into pulmonary cirulaiton, muscle wall sown restrictions flow + DA closes.

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33
Q

describe thermoregulation in neonate?

A

brown adipose tissue - responsible for non-shivering thermogenesis on hypothalamus neonates in first 5 hours
colostrum - source of energy in first 12 hours
energy expandable via attempting to stand

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34
Q

desicbe brown adipose tissue and its advantages?

A

1-2% of fetal wight at term - but can be repsosiable for 100% of heat generation post naturally
formed near kidney - activation of non-shivering thermogenesis at birth due to sympatahtis signals

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35
Q

describe the anatomy of mammary glands?

A

modified skin glands (sweat)
both sexes but develop in females after birth/
Age related structure - rudimentary duct system = secretary alveoli develop.

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36
Q

name and number the mammary glands of diffenrt species?

A
bitch = 8-10 - thoracic-abdominal-the groin area (inguinal)
Mare = 2-4 - udder, 1 pair, inguinal 
sheep = 2 - 1 pair, inguanil 
Pig = 8-12 - 6-7 pairs, thoracic-abdonomal-inguinal
Cow = 2-4 - 50Kg!! hind quater, fore quieter
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37
Q

describe the bovine udder?

A

purpose = lactation- supermammroy teats common on hind quarters.
suspensory apparatus supports the weight of lactating udder
consists of: medial + lateral laminae, aponeurosis of external adom.oblique muscle

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38
Q

what does the bovine udder consist of?

A

tunica flava, linea abla, medial laminae, Lateral laminae inter-mammary groove

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39
Q

name the internal features of bovine glands?

A

glandular parenchyma - simple cuboidal secretary epithelium near capillary bed.
myoepithelial cells surround alveoli + eject milk into branching duct system.
teat canal or papillary duct - closed in-between milking

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40
Q

describe the anatomy of the bovine teat gland?

A

milk duct
Teat cistern / gland cistern
lactiferous sinus

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41
Q

describe how the closure of the teat occurs?

A

for defence to microbial influx
mucosa in region involved in immuno-survallance.
1) smooth muscle sphincter - closure of teat
2) teat canal and teat sphincter close
mucosal surface of teat seals and folds.

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42
Q

name the main arterial supply for teat?

A

extended pudendal artery
500L ion blood : 1L milk
passes form inguinal canal/sigmoid flexure splits into cranial n caudal mammaery arteries.

43
Q

name the two venous triage veins for teat?

A
external pudendal vein 
subcu abdominaal (milk) vein
44
Q

describe the lymph drainage of teats?

A

removal of excess tissue fluid.
flows through superficial inguinal lymph nodes
the larger lymphatic vessels are very superficial + can be palpated.

45
Q

what is mastitis?

A

enlargement of mammary lymph nodes (deep inguinal nodes will also be enlarged)

46
Q

explain the nerve supply for mammary glands?

A

L1 - leads to abdominal cavity
L2 - branches off to craniel teats
L3/L4 - caudal teats
S2-4 - back of mammary gland/sac

47
Q

explain the milk let down reflex?

A

oxytocin released form hypothalamus

milk production dependent on levels of prolactin but also regular removal of milk

48
Q

describe the historical different between active + inactive mammary glands?

A

1) - Number of active alveoli decrease
2) increased in CT component of gland
3) gland never regresses to eat it was prior to pregnancy.

49
Q

describe the regulation for lactation?

A

animal gets pregnant - accelerated duct devolpmemt second half of pregnancy - lobular-alveolar devoplet.
increase oestradiol causes increase in progesterone and removal.

50
Q

describe lactogenesis 1?

A

alveolar sections become apparent in last week before parturition. - change form extracellular to milk - pre-colostrum

51
Q

describe lactrogeneis 2?

A

alveolar secreto can NOT be re-absorbed due to epithet tight junctions - proper milk lactation.

52
Q

what does the removal of progesterone cause in lactation?

A

allows onset of active lactation - direct stimulation rise in prolactin

53
Q

describe milk composition in dairy cow?

A

proteins (caseins, whey) levels drop after first day
ions (Ca,P,Mg) levels drop after first day
Lactose (INCREASE after first day)
fat - levels drop after first day
IgG (colostrum) levels drop after first day

54
Q

name the two near-endocrine reflexes in milk lactation?

A

Milk let down reflex
milk production reflex

stimulations lead to posterior pit section of hormones - oxytocin + antidiuretic
aswell as Ant Pit = prolactin

55
Q

what is the milk let down reflex?

A

1) oxytocin released from posterior pit
2) oxytocinR effect myoepithilium cell and causes Mechano-receptors to activate ant.pit for release of prolactin to activate more milk production

oxytocin release in the cow, showing prolonged pulse of prolactin in plasma during milking on Days 2 and 3 postpartum

56
Q

how can the milk let down reflex be conditioned?

A

positivily and negativitly - Conditioning can occur and affect oxytocin release

57
Q

how can adrenaline effect the milk let down reflex?

A

Adrenaline: reduces mechanoreceptor and myoepithelial cell stimulation

58
Q

how can metabolic hormones be used for onset of lactation?

A

lactation - stimulated by Prolactin, growth hormone, Thyroxin, Insulin, Cortisol, PTH, Calcitonin, Vit. D

59
Q

what is involution and how does it occur?

A

it removes the milk-producing epithelial cells when they become redundant at weaning.
tissue atrophy - occurs due to lack of milk removed by neonate (drying off)

60
Q

what hormones control gestation?

A

Prl, placental lactogen, GH, Cortisol, E-17b(Ovarian-produced 17B estradiol (E2)), Progesterone

61
Q

how does robotic milking increase milk yield?

A

unilateral frqerny milking increases the yield in half udders in holstein and goats

62
Q

what is an FIL?

A

FIL = feedback inhibitor of lactation
an autocrine local peptide suppressing milk synethsis
if there is no demand (= no removal)

63
Q

what is abortion?

A

premature expulsion from uterus of non-viable products of conception

64
Q

what is a premature birth?

A

premature expulsion form uterus of viable products of conception

65
Q

what is a still north ?

A

delivery of a fully formed dead neonate

66
Q

why is an abortion so important to a farmer/vet/anyone involved?

A

1) health and welfare of dam and foetus (5 freedoms)
2) ecomincs - individual cost of abortion = dairy cow =ÂŁ600
sheep = ÂŁ70
beefcow= ÂŁ800
3) legal - abortion/calving tales place = 271 days after - met report abortion within 24 hours
4) zoonotic - transmosisn of disease to humans - must protect ourself - must discard of birth up to 6 weeks

67
Q

how to control abortions?

A

Non-infectious - indirect - biosecurity, vaccinations, bio containment- disinfectant, isolate the animal, breeding,, treatment v culling
disease control v disease free

68
Q

what to expect when an abortion occurs?

A

clinical - no clinical signs of an abortion prior.
multifunctional - more that one infectious agent, nutritional, good food provided.
bovine - chlamydia abortus (EAE)
toxoplasma gondii! common!!!!

69
Q

what breeding season do mares have?

A

seasonal polyoestrus - April - spetemebr
anoestrus - during winter months
long day breeders.

70
Q

what occurs in anoestrus?

A

pineal gland produces melatonin which suppresses hypothalamus producing GnRH, less GnRH does not stimulate ant.pit FSH release so everything is suppressed.

71
Q

what occurs in loner days in mares? more sunlight?

A

more melatonin produced by pineal gland - more GnRH - ant.pit increase FSH/LH production - increased ovary activity.

72
Q

what hormones are used for early season manipulation?

A

synthetic progesterone

human chronic gonadotrophn (hCG) - hasten first ovulation of breeding season

73
Q

names some pre-breeding checks in mares?

A

age, history, general reproduction , physical exam , BCS, disease free etc

74
Q

how is the external genitalia assessed?

A

perineum, vulvar seal, discharge. examine cervix and vestibules.
clit swab - micro tip for CEM, transrectal palpation + ultrasound.

75
Q

what is Caslick’s Procedure?

A

dorsal portion of vulva struture shot only ventral portion open
reduced vaginal contamination
can re-open prior to foaling

76
Q

describe the mare oestrus cycle?

A

21 days
5-6 days oestrus
24-48hrs ovulation occurs before end of oestrus
lutenisising hormone - causes primary follicle to mature and ovulate.
redness of vulva and external signs of oestrus - teasing with saliva
ultrasound + palpation = uterus + cervix = soft and relaxed

77
Q

how do some hormones manipulate induction of ovulation in mares?

A

1) hCG = has LH activity, follicle ovulation within 48hrs at injection
2) GnRH - when follicle induces ovulation with 48hrs of introduction of a subcutaneous implant, stimulates release of FSH and lH from Ant.Pit gland

78
Q

describe artificial insemination in mares?

A
advantages - one ejactulate divided into several insemination doses 
- more beed to remote stallions
- prevent STD
- avoid breeding injuries 
disadvantages - can be expensise
- increased skill required
- risk of injury to human
- not for thoroughbreds (TBs)
79
Q

how does artificial inseminaiton work?

A

semen delivered into uterine body using plastic catheter via vulva through cervix to tip of uterine horn
needs less semen then .

80
Q

what is an embryo transfers?

A

use multiple embryos per season for success
technically demanding
expensive
not TBs

81
Q

describe the pregnant mare?

A

duration = 320-365days (embryo implant at 16 days)
want to avoid twin pregnancy - use ultrasound to check up.
blood hormone levels: progesterone not reliable enough
oestrogen sulphate levels elevated after 100 days pregnancy.
needs nutriaonl support - gradually increase in last 3 months

82
Q

what occurs in a mare pregnancy loss?

A

usually loss by 49 days
placental dysfunction - most common cause of abortion,
premature udder devoplement and lactation.
non-infectious - twinning
infectious - placentitis - abortion

83
Q

describe equine parturition?

A

24-48hrs - waxing up before
few hours before - relaxation of vulva, relaxaion of sacrosciatic ligaments, cervical softening, tail head drop
mammary gland secretions occur
normal parturition - preparation of foetal expulsion - sweating, restlessness, mild colic,

84
Q

describe stage 2 parturition of the mare?

A

uterine and abdominal contractions normally takes less than 20mins
causes rupture of chorionallantois, loss of allantoic fluid, espouse of amniotic memebrane

85
Q

describe an emergency in a mare parturition?

A

premature separation of placenta, RED bag delivery - chorion separates form endometrium, chorioallantois passed without rupitng: palpate foal inside, need to rupture immediately.

86
Q

describe stage 3 mare parturition?

A

uterine contrition, mild colic, normally 3 hours,
oxytocin therapy, fluid distention.
examine membrane for integrity.
normal placenta ( looks like ‘F’)

87
Q

what is Dystocia?

A

presentation of placenta - longnitudla or transverse, sacrum, right ilium, left ilium or pubis
normal is dorsosacral
Dystocia = malposture
Abdominal posture - derived from head/neck very common

88
Q

what causes Dystocia?

A
foetal malpresentation
foetal malposition 
foetal malposture = most common
foetamaternal disproportion 
congenital anomiales
twinning
uterine torsion
89
Q

how is Dystocia treated?

A

manipulation of foetus to ensure successful delivery, after repulsion
limited time tho

90
Q

what must you do post partum - foal assessment?

A

immeduaoty leave, undisturbed, allow bonding, if needed: remove amnions from mouth/nose etc
treatment of umbilicus - potential route of infection
0.5% chlorhexidine solution preferred
repeat every 6-8hrs for several days

91
Q

give a rough timeline of foaling?

A

mare - gestation = 335 days

  • second stage parturition - 20-30 mins
  • placenta expelled < 3hrs

Foal - suck reflex = <30mins

  • nursing = < 2 hrs
  • passage of meconium = < 4hrs
  • urinaiton = <6-10hrs

standing = 1 hour
nursing = 2 hours
placenta out = 3 hrs

92
Q

what can you do if there is no suckle from foal?

A

no colostrum gets to foal, implications for immunity.

means no nutrition + hydration - 2hrs of glycogen, retained meconium - colostrum has a laxative effect

Colostrum 1 - vital for passive immunity 1.5L per hours needed. contains IgG flow into intestines - used for pinocytosis of IgG, rapid lost after 12 hours onwards.
if passive immunity is not delivered - 2 month window for which foal has an increased infective rate

93
Q

what is a plasma transfusion?

A

1/2L of hypermure plasma - pathogen free. maternal/geilding harvested plasma.
Re-check after administration

94
Q

what is Meconium retention?

A

meconium - firm dark pellets in intestine that cause tenesmus/colic.

95
Q

what is treatment for meconium rentention?

A

emnamus = human property, soapy water with soft tube

96
Q

how much feed should an orphan foal get per day?

A

BW/24hrs on day one
slowly increased to 20-25%
volume of feed depends on frequency- maximum 300ml initially

97
Q

describe foal ongoing care?

A
umbilicus stump - dried up within 24hrs, falls off later
Feeding - starts to nibble things 
weaning - often 4-6 months
vaccinator - 6 months
deworming - 6 months
98
Q

what is the post partum period in cow?

A

calving - 3 months for resumption - dominate follicle growth, LH pulsailty, oestrus cycle etc
takes first 6 weeks of postpartum period to invite the endometrium to regenerate.
1) uterine horn revers to normal size
2) endometrial restration.
3) ultrasound scans of post partum ovaries showing resumption of ovulation.

99
Q

explain the events of post partum resumption of ovulation

A

1) FSH rises for follicle wave emergence
2) dominant follicle selection as normal
3) GnRH pulsility increase to replusion LH stores + stimulate LH pulses.
4) follicular oestradiol production + rising oestradiol in circulation.
5) induction of 1st gonodattoph surge post partum via oestradiol positive feedback

the high stripe profiles before calving led to a down regulation of GnRH/LH pulses.

100
Q

what is the ovarian status before parturition?

A

low FSH
absent LH pulses
small central follicles only, no dominat follicles

101
Q

do all cows have a quick PP recovery?

A

yes, recovery of FSH and dominant follicle growth

first ovulation depends on breed health and PP LH pulsatility.

102
Q

how does dominant follicle growth occur?

A

frequent LH pulses.

103
Q

describe the post partum interval in beed cows?

A

interval to 1st ovulation + anoestrus period in beed cow depends on

1) BCS at calving
2) sucking frequency
3) presence of the calf