branimira Flashcards
maternal causes of dystocia
failure of expulsive forces (uterine or abdominal causes)
primary uterine inertia
Are the onset of birth, (bitch, sow)
Fetus remains in intrauterine position
(uterinecontractions fail to be initiated)
Causes:
myometrial defect (overstretching, infection, degeneration, systemitc illness, hereditaty, small litter size)
biochemical deficiencies (E-P ratio, oxytocin, PGF, relaxin, Ca or glucose def)
oligamnion
premature parturion
envoronmetnal disturbances
condition - obsetiy/ malnutrition
Therapy : hand vaginal stimulation (Ferguson reflex), extraction of fetuss
secondary uterine inertia
consequence of another case of dystocia
at first contractions are normla by thten myometrial exhaustation
cause = uterien damage or prolapse
therapy = eliminate cause, extract fetus, uterotonics in bithcn adn queen
abdominal causes of dysotica
Inability to strain
Causes : age, pain, debility, diaphragmatic rupture, tracheal / laryngeal damage
obstruction of birth canal
Bony pelvis
= Congenital = developmental abnormalities of the pelvis are generally rare in animals
= Acquired = fracture, diet, immaturity (juvenile pelvis), neoplasia, disease – exostosis (periostitis)
Soft tissue
= Vulva = congenital defect, fibrosis, immaturity
= Vagina =congenital defect, fibrosis, prolapse, cystocele (bladder, prolapse in vagina), neoplasia, prevaginal abscess, hymen
= Cervix = congenital defect (duplication – cervix duplex), fibrosis, failure to dilate – narrow cervical canal (4 degrees)
= Uterus = torsion, herniation, adhesion, stenosis of the horn or corpus
narrow pelvis
interfere with the passage of a normally developed fetus
More common in non selective breeding + dwarf breeds
Pelvic inlet of the achondroplastic breeds of dog is flattened in brachycephalic breeds, is a common of dystocia
Therapy : mostly cesarean section, fetotomy
immature, juvenille pelvis
A
more common in sows, goats and cattle
Prematurely mated animals (the pelvis is not completely ossified)
Rachitis (most often in sow)
Therapy : mostly cesarean section, fetotomy
narrow vulva and vagina
Most often in primiparous (heifers – overfat body condition)
o Prematurely mated animals (juvenile females)
o Insufficient serous infiltration of the soft parts of the canal
o Scar tissue, connective tissue – bar, wounds, persistent hymen (foals), congenital stenosis, edema of the vulva due to venous stasis
o Simultaneous appearance of a narrow vagina and vulva is possible
o Therapy : mostly operation – episiotomy
narrow vertical canal
- Mostly in cows, sheep and goats
- Disorder of the opening stage .
- Hormonal insufficiency + Insufficient serous infiltration
- Incomplete dilation of cervix in the ewe and doe goat (ringworm) -commonly associated with prolonged gestation and hypocalcemia, hypophosphatemia
- Consequence of uterine torsion
Scar tissue, wounds, neoplasms - Protracted labour – 6-12 hours after rupture of the fetal membranes, involutionary processes
- Degree of incompletely open cervix according to Götze
therapy: medically, manually
= denaverine hydrochloride, misoprostol, fetotomy
stages of cervical canal (narrow cervical canal according to goetze)
1 =ring like cervix that adheres closely to the fetus, its hard and easily rupture during extraction of the fetus
2 = only legs or head pass through the cervical canal
3 = only 2-3 fingers or fists can be inserted into the cervical canal
4 = cervical canal is closed (uterine torsion > 180 degree)
torsion of gravid uterus
Rotation of pregnant uterus on its longitudinal axis to the left/right which leads to narrowing of the birth canal
Cow, rarely mare, small ruminants
Cause
disposition (cattle) – anatomical relations, insufficient fixation of pregnant uterus
Predisposing factors
excessive movements of the foetus/dam, decreased volume of fetal fluid, fall, kicking, relaxed ligaments, fetal overweight, cow tied in the barn for long period
Features
ACW and CW (90-360o) <45 degrees is sufficient to result in dystocia
Either precervical or postcervical rotation
Torsio cornualis/ torsio cornuum uteri – place of rotation is one uterine horn or part of horn in small multiparous animals
Signs
parurition not progressing, uneasiness and restless, vulvar lips uneven
Diagnosis:
Vaginal: conically closed, shrinkage of front part of vagina, rotation of mucosa felt
Rectal: palpation of twisted horn and broad ligaments
Prognosis:
depends on degree of torsion
Therapy
return the uterus to its normal position
direct: to uterus with foetus
o with extraction – turn foetus opposite to the torsion
o kamer method – try to encourage the foetus to turn/turn ourselves
o cämmer’s torsion fork with canvas cuffs – use of detorsion rod to correct a uterine torsion
o auer-shreiner method: 3 forces simultaneously on uterus and foetus
o snöborgs method: press abdominal wall (similar to above)
indirect: directed to mother’s body (in direction of torsion)
o hold uterus in place and turn over cow (rolling)
C-section: when other methods don’t work, at long duration, foetus is dead and uterine rupture is possible
endometritis in mares
Inflammation of uterus, differs in etiology, clinical manifestation and duration
The most common cause of subfertility and infertility
Every mare 5-15 years old, mates or AI in 3 consequetive estrus without conception thoroughly suspicious on endometritis
physiological endometritis after mating
PMIE
chronic endometirits
degenerative endometritis
physiological endometritis
Immediately after mating for AI
Uterine response on bacteria and proteins from semen
Resistent uterus overcome inflammation in 6-12h
Healthy endometrium overcome infection in 6-12h
Time frame 120 – 150h before embryo reaches uterus
PMIE
Predisposing factors
= Inadequate evacuation of inflammation products, inadequate lymphatic drainage of uterus
= Poor contractibility of myometrium
=Bad overall conformation of mare
=Hormonal disbalance
occurs due to failure of natural defence mechanism
signs = vaginal discharge and inflammation
histroy = failure to conceive, irregular cyclicality
Treatment in estrus and post estrus with monitoring of mare – individual approach - flush uterus, repeat until clean
20IV ocytocin post flush
flush 4-6h post mating
cloprosenole but can influence CL
diagnosis of endometritis
Clinical (anamnestic, vaginal, rectal ultrasound)
Ultrasound – accumulation of fluid in uterus
= Fluid in utero 6h mating – normal
= Fluid in utero 12h or more after mating or AI = worrying
= Fluid in utero 24h or more after mating or Ai =endometritis
Laboratory (cytological, bacteriological)
= Cytological smear of endometrium or low volume flush
= Bacteriological cultivation of microorganism
=Proper evaluation based on combining both tests
= If in doubt, cytological smear more significant (number of neutrophilic leukocytes)
prevention of PMIE
Decrease number of mating or AI
Avoid mating out of full season
Ultrasound monitoring of ovulation
Start therapy immediately Induce ovulation with hCG or synthetic GnrH for LH (buserelin and deslorelin)
AI with extenders containing antibiotics
Minimal contamination technique
chronic endometritis
Untreated PMIE become chronic endometritis
cause = poor conformation, trauma, inadequeate vulva/cervical sphincter
bacteria = strep equi, e.coli, p.areuginosa, k.pneumonia
3 natural barriers:Rima vulve, vestibulo-vaginal ring and cervix
Diagnosis: history, vaginal, rectal, US, endoscopy, cytology
therapy:
surgical correction of anatomical defects (cassock, correction of urethral flow and correction of laceration)
ATB, flushes
for chronic mycotic = clotrimazole, amphotericin
pyometra as consequence of chronic endometirits
Multicausal etiology
o Fibrotic cervix, adhesia of cervix
o Chronic endometritis
No visible signs
Intermittent purulent discharge
Irregular cyclicity
Poor prognosis for future fertility
Uterus permanently damaged
Endometrium replaced with granulation tissue
Atrophy and fibrosis of endometrium
Recurrent disease
endometriosis
Direct link to early embryonic mortality and cervical fibrosis
Senile atrophy of uterine glands older pluriparous mares (>15g)
Endoscopic and PHD finding
it’s a degenerative chronic condition demonstrated by fibrosis within the endometrions
- irreversible
- severity increases with age
- diagnosis = biopsy
- it’s caused by growht and spread of tissue similar to the endometrium or uterine lining outside of the uterine cavity
endometrial cysts
Lymphatic and real endometrial (usually due to drainage of lymph)
Doesn’t involve direct in fertility
Could disturb embryo mortality
Laser and caterisation during endoscopy, if indicated
cause of infertility in cows
functional ovaires
displaying oestrus behaviour
narrow vagina
ovulation disorders
abortion
dystocia
detachment of placenta
freemartinism
most common non-inflammatory condition - 92% of heifers born to bull twins
results in infertility involving tubular reproductive tract
what are chimeras
individual animals that contain two cell types originating from separate zygotes
signs of freemartinsim
heifers have the bullish appearance and behaviour of male animals
vulva is small and shrivelled with very pronounced clit, urination is strong jet directed upwards
internal repro organs abnormal
rectally: cervix and uterus often missing
least masculinised form more common - hypo plastic ovaries, short vagina and absent cervix
cause of freemartinism
day 28-30 of pregnancy = fusion of chorioallantoic part of placenta meaning common blood supply between twins
exchange of humeral and cellular elements between fetes –> 2 chimeras
testicular development occurs before ovaries I cows + antimullerian hormone from male inhibits growth of female
RBC, WBC, antimullerian germanitave embryonic stem cells androgens enter the female blood stream
50th day of feral development = initial freemartin development
75th day = masculinisation
diagnosis of freemartinism
clinic exam: rectal, length of vagina test
<7cm = freemartin, do chromosome testing if 7-14cm
false positive if persistent hymen
false negative if normal legnth
PCR = finds XX and XY in same animal, fast and accurate
karyotyping = blood lymphocytes in metaphase - spread and examine for XY cells
skin grafting - freemartin heifer will accept skin from male twin
prognosis of freemartins
most female cattle that are blood chimeras are often sterile freemartins
barren so use for fattening - not for mating
hermaphoriditism
mixing of sexual characteristics of both sexues in 1 individual
type of hermaphrodism
ambiglandular
testciular
ovarian
ambiglandular
bilateral = 1 testis + 1 ovary or 1 ovartestes on either
unilateral = testis and ovary/ ovotestes on 1 side and ovary or test on other
alternate = testis on 1 side, ovary on the other
rodents and pigs
testicular
in goats, sheep, cattle and horse
only testis on both sides but external genitalisa resemble female
cause = androgen insensitivity
XY male and production of testosterone normal but due to intracellular androgen insensitivity - mesonephric duct system doesn’t develop
vagina = short or normal, no cervix, small or absent uterus and testes in normal ovary position
maybe inherited in cattle as X-linked trait
ovarian
cause = enzymopathies in steroid conversio
chromosomal factors
heterosexual twins in cows
more rare than testicular
congenital repro problems cow
ovarian hypoplasia
congenital lesions on ovaries
abnormalities of uterine tubes
aplasia uteri
aplastic cervix
cervix duplex
uterus didelphys
vagina subsepta
hymen feminis persistens
ovarian hypoplasia
hereditary and recessively transmitted to offspring
if unilateral - can conceive
if bilateral - not cyclic
partial = can conceive but will have a small reserve of follicles and stop cycling before being ready to mate
signs = small functionless ovaries with undifferentiated parenchyma, infantile genital tract and not cycling
congenital leiosns on ovaries
very easy to diagnose
hypoplastic ovaries don’t respond to eCG or GnRH so no oestrus
don’t use bulls with small, asymmetrical testes for breeding
cervix duplex
1 = duplication of lumen - each horn connects to vagina by separate canal-normal conception
2= 1 cervix opening in to a double of uteri sometimes 1 channel not patent
lower results with mating/AI
bulls transmit to 3-9% of offspring so exclude from breeding
uterus didelphys
complete absence of fusion of 2 paramesonpehric canals
AI in ipsilateral horn-conception and AI possible
vagina subsepta
= dorsoventral post cervical band and vertical vaginal bands
if adjacent to cervix - can interfere with sperm, calving or placenta passing
diagnosis = vag exam and palpation
therapy = pull as causally as possible and cut with scissors or fetotom knife
acquired repro problems co
ovaritis
ovarian neoplasia
lesions of uterine tube
mucometra
uterine tumours
uterine adhesions
urovagina - cow
in cachet and old cows
prevalence in carols and holstein
pelvic and uterine ligaments loosen, anus and vulva moves forwards and vulva lies horizontally
vagina pulled cranially and hangs over edge of pelvis - urine leaks out of vulva and some goes into vagina
sometimes covers cervix –> endometritis
ovarian cyst cow
A
cysts = diameter > 2.5mcm but continues to grow and persist in absence of CL from follicle that didn’t ovulate (10d+)
benign = look like follicular cysts but don’t inhibit cycle/ovualtion/waves. CL present
most cysts disappear by 60d pp but some persist = chronic
how to help with anovulatory conditions in cattle
improve energy status during transition period
prevent disase
decrease frequency of suckling to 1-2 x1d in beef cows
GnRH agonist, prostaglandins or progestogens
differentials of ovarian cysts cattle
corpus hemorrhagicum
vaculoalted LC
non-ovarian cyst
abscess
tumour
types of ovarian cyst cattle
follicular
= thin wall, fluctuating, progesterone <1ng/ml. 15-45d post calving
luteal
= wall > 3mm, progesterone >1ng/ml formed from unovulatoed follicle and theca cells luteinise or formed from follicular cysts
signs of ovarian cyst cattle
follicular = 80% anestrus, unequal esters or persistent anestrus, masculinisation
luteal = anestrus
risk factor of ovarian cyst cow
dystocia, RFM, NEB, obesity, increased temp, older, feeding oestrogen type components
cause of ovarian cyst cattle
neuroendocrine imbalance
therapy of COD cattle
follicular
= treat, don’t wait for regrression
= GnRH - leads to increase LH and lutenisation of cyst (oestrogen -> progesterone)
= then PGF2a 7-10d later + increase P4 - restores hypothalamic response to estradiol and ovualtion occurs
= 72% cows regain cyclicality in 28-30d post GnRH
= 20% remain in anestrus - P4 remains low during lutenisation and response of hypothalamus to estradiol doesn’t change
= intravag progesteagen for 9-12d = cyst regression + grow of follicular wave. Esters 7d after removal
= cyst aspiration
luteal
= PGF2a most effective
= GnRH or hCG good, but unsure what type of cysts
= GnRH then PGF2a 7-9d later, don’t rupture - haemorrhage and adhesions
prevention of ovarian cyst cow
decrease stress, treat infection, prophylactic GnRH 12-14d post birth
no effective treatment for multiple cysts so cull
absent or delayed ovulation
oestrus and ovualtion sized follicle that doesn’t ovulate and regress or ovulates late (normal 25-35h after esters)
delayed = 48 h between statrt of esters and ovulation
cause = insensitivity of hypothalamus to estradiol, weak LH surge
aetiology = NEB, heat, stress, increaction, fast metabolism
delayed ovulation = decreased conception due to old oocyte - improper fertilisation, poor development potential old sperm
Changes in uterine tube environment (slow passage of zygote)
-prevention = GnRH with/before AI
ovarian atrophy
small, hard, smooth ovaries without any formation
cause = prolonged non-stimulation of ovaries by hypothalamus - pituitary gland
aetiology = def Ca, P, Cu, Co, Fe, I , vitamin A, O, E, malnutrition, chronic disease, hoof problems, parasites
physiological atrophy = sterile
atrophy is high producing = atrophy lactations
therapy = treat primary cause GnRH, eCG, hCG, CIDR, vitamins, minerals, antiparasititics
don’t confuse with hypoplasia of ovaries (congenital and irreversible) –> will be no reaction after hormones, no germinative layer
bartholin gland cyst
= under mucosa of vestibule of vagina 2-10cm big, unilateral in older cows
cause = atresia/obstruction of excretory ducts
signs = disturb urination, interfere with mating, vaginitis
DD= tumour, prolapse, absecess
if puncture - amber liquid
treat = hold top of cyst and cut with scissors along wall of vagine rinse inside with 10% betaine
will reoccur if just punctured
penumovagina
vulva not acting as a seal, aspiration of air and maybe faeces
leads to dilation of vagina and maybe uterus and bacterial contamination
cause = aging, vulva conformation, BCS, trauma
treat = none if mild, vulvoplastiy.caslick, treat underlying cause - BCS
AI to increase subfertility
prognosis = severe cases unlikely to breed successfully
RBC
= normally cyclic cow with no clinical abnormality which has failed to conceive after 3 successive insemination
pathologic conditions of RBC
subclinical endometritis
= chronic uterine damage
luteal deficiency
= insufficient progesterone so suboptimal growth of blastocyst so not enough IFN-1 for luteloysis
delayed ovulation
= extended follicular phase and decrease signs of oestrus
- increase progesterone concentration > allows follicular growth but postpones LH surge
- 2 wave cycles = old follicles
treatment of RBC
intrauterine ATB 10-12h post insemination
- uterus can recover before embryo arrives in uterius at day 4-5
- give GnRH at time of insemination
cause and factors of RBC
cause = unclear but mulitfactorial
-> cow, bull, environment
factors: age, genetics, infection of repro tract, nutrition, embryo mortality
trauma in small rum
sheep= very resistant, maybe unnoticed
towards end of pregnancy - distended abdomen >5% abortion rate
most common cause = 3Ps
protector dog = too aggressive
pastor = too many sheep in truck
passage = narrow aisle
sheep need 50cm each at feeding station
pseudopregnancy in goats
hydrometra, mucometra, cloud burts
accumulation of aseptic secretion within uterine lumen
signs = cyclic activity stops due to spontaneously persistent CL, abdomen distension, cloud burst at time of expected delivery, does looking for kids
diagnosis = US - no foetus or placetnomes and fluid in uterus
therapy = prostaglandins 2x in 12d
pregnancy toxaemia
cause = nutrition, toxemia, multiple fetus, BCS
unable to eat enough –> fat related –> converted to FA + glycerol for metal growth –> KB near birth –> abortion
toxemia due to too much metal metabolic products
signs = lethargy, muscle tremors, grinding teeth, opisthotonus, ataxia, coma, hypoglycaemia, ketonuria, increased BHBA, decrease Ca, increase K
therapy = bicarbonate, Ca, glucose precursos
No IV glucose due to hepatic lipipodsis + end of pregnancy insulin resistance
No PO glucose because digestion in ru,en causes FA formation
pseudolactation
physiological in bitch
prevalence = afgans, beagle, boxer and rare in cats
usually 1-3 m after oestrus but also 3-4 d post OVH in diestrus
pathogenesis of pseudolactation
physiologically,i diestrus is similar between pregnant and non-pregnant bitches
trigger= progesterone decrease and prolactin increase, increase tissue sensitivity to prolactin
- different molecular types of prolactin with different bioactivity
- prolactin secretion in pituitary is under tonic inhibitory contorl of hypothalamus, mediated by direct inhibitory action of dopamine, or indirect serotonin (dopamine secretion suppressant)
