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)
signs of pseudolactation
6-8 weeks after estrus and can last 30-90d
covert = no signs, physiologic condition
overt = divers signs
behavioural changes, physical changes in caudal mammary gland, aggression
often self limitig but can occur after every oestrus
complications and dd of pseudolactation
rare - vomiting, anorexia, PUPD, tumours, mastitis, CEH
DD = rule out pregnancy, mastitis, tumour, pyometra
diagnosis of peudolactation
signs and histroy
hormonal tests no due to specific physiology of sexual cycle of bitch
treatment of pseudolactation
mild = no treatment, prevent maternal behaviour, elizabethan collar
therapy if strong bevhaioural changes lasting longer than 4 weeks
drugs = antiprolactinemic, serotonin antaognist with dopamine eeffect I hgih dose (metergoline)
- dopamin agonist are prolactin inhibitors that exert effect by direct stimuatlion of dopamine D2 receptors
eg caergoline 5ug/kg PO for 7-9 d pergolide, bromcriptine
ovariohysterectomy is anestrus
no milking, tranquilliser but not phenothiazines
treat all bithces due to risk of mamary gland neoplasm
what is feline mammary fibroepithelial hyperplasia
benign, progesterone assocaited fibroglandular proliferation or 1 more more mammary glands
can occur in males or females
most common in, intact cats 6m-13yr
when = 1-2 weeks after estrus or 2 w after hormonal therapy
pathogenesis of FEH
not completely understood
growth + development of mammary gland under progesterone control
-> progesterone in stromal and epithelial cells –> activation of specific cascade –> mammary gland proliferation
-> maybe changed regulation leads to disturbed response to progesterone
progesterone –> ductal branching
estrogen –> ductal elongation and bifurcation
progestogens cause stimulation and proliferation of epithelial cells and ductal canal to hyperplasia
high proliferative index
blood progesterone in normal conc
pathomorphological characteristics of FEH
firm, well-circumscribed unencapsulated mass, solid and smooth
possible ulcerations and necrosis
micro=profieration of glandular, fibre - epithelial elements
therapy and prognosis of FEH
prognosis = good but relapse possible if no OBH
supportive therapy
treatment:
- OVH or ovariectomy = gold standard –> regression in 3-4 week, if not mastectomy
agleprisoton = competitivee progesterone antagonist 10mg/kg SC 1st then 3rd day, control day 7 repeat if needed, regression within 4-8 weeks
dopamine agonist for suppression of lactation
cabergoline for 5-7 days
bromocriptine 0.25mg/kg PO for 5-7 days side effects = ticks
clinical findings of FEH
15-18cm excessive enlargement that appeared very rapildy
can be: bilateral whole chain enlargement asymmetric (non-pregnant) solitary mass in any gland
skin = tense and erytheamtous
palpation = firm, compact conssitency soft, gelatinous mass
lab = normal
large masses = problems walking
Greg queen = no milk, weak kittens
complications of FEH
mastitis in lactating queens
ulceration due to overstretched skin
maybe hemorrhagic/purulent exudate
increase temp, lethargy, anorexia
LN involvement
diagnosis of FEH
signs = spread of development
biopsy = FNA or excision - large amount of mitosis = false malignanyc
US - increased echogenicity
DD = neoplasia, FEH = bigger and softer
congenital abnormalities in bitch
ovarian genesis rare and only affects fertility if bilateral
ovarian dysplasia in bithc with abnormal number of chromosomes
intersex - pseudohermaprhodites
vulvar hypoplasia and perivulvar deermatitis
transmissible venereal tumour dog
affects vagina and external genitalia of bitch and penis in dog
transmission through coitus and sniffing and licing etc
lesions = friable, multilobulated max size after 5-7 weeks and can regress spontaneously within 6 months
metastasis uncommon
therapy = surgical debunking and them vincristine for 3-6 seeks
intratumoural injection with vincristine and interleukin 2
cystic endometrial hyperplasia - bitch
acute/chronic post estral disease of adult intact bitches leading to inflammatory exudate in uterus
cause = repeat exposure of endometrium to progesterone
predisposing = 2 month diestrus
pyometra
progesterone mediated uterine disease occurring during diestrous
bacterial infection with opportunistic organisms from vagina secondary to CEH
most common organism = e.coli
types of pyometra
open
= 4-8 weeks post estrus, vulvar discharge, less systemically ill
closed
= abdo distension, minimal discharge, more systemic signs
signs of pyometra
fever
hypothermia
dehydration
lab and diagnosis of pyometra
lab
= neutrophilic (penia if endotoxemia)
= normocytic, normochromic aneamia
= WBC left shift
= azotemia, increased ALP and ALT
= hyperglobulinemia, hypoalbumineam
diagnosis = gen and gyno exam
x-ray or us
therapy for pyometra
ovariohysterectomy
medical =have to be of breeding age, vital to program, open Cervi and not systemically ill
PGF2a dinoprosvt 2x 1d cloprotenol or alphaprostol fluids, pain relief, atb antipgroestins = no sidde effects compared to prostaglandins
split estrus dog
most common at first and second estrus
signs = vulvar swelling, serosanginous discharge, no ovulation, follicles regress and proestrus signs disappear
cause = premature atresia and regression of follicles due to insufficient secretion of LH
-> normal estrus 1-3 weeks laterr
-> progesterone remains basal despite showin estrus signs
mate at correct time in relatio to OV
vaginal prolapse dog
= protrusion of oedematous vaginal tissue into vagina lumen and through vulva lips
cause = unknown (no hyuperestrognism) but is due to estrogen sitimualtion during estrus and protestrus
1= slight.moderate eversion of vaginal tissue through vuvlar lips
2= prolaspe of cranial floor and lateral walls trhough vulvar lips
3= prolaspe of entire vaginal circumference as a donnut shaped mass
signs = discharge, dysruia, anuria
treatmet = can regreess spontaneously so keep clean and dry
surgery = for type 3 - circumferential excision of prolapsed tissue -> can recur so OVH
pyometra queen
ess common than in bithces
bacterial infection of uterus due to hormonal changes in cats
signs = variable, decreased appetite, PUPD, vomiting
pus contianing blood is open cervix
therapy = OVH
medical treatment maybe if open cervix not severely ill and for valuable breeding female
endometrial biopsy mare
biopsy = taking piece of uterus surface to detect inflammation or degenetation
indication = prepurchase exam, barren mare, past infertility, abortion, pyometritis or mares needing repro surgrey
when = estrus - cervix in open and more easily penetrated and mare more resistant to endometritis
diestrus = endometrial glands more active and may give better picture of their function
categories of endometrial biopsy mare
I : (NONE) healthy mares, no pathologic chcanges or any existing changes foaling rate 80-90%
IIA: (MILD) small changes, slight to moderate inflammatory changes, 50-80%
IIB: (MODER)figrotic changes are more severe, inflammation is more widespread, 10-50%
III: (SEVERE)severe changes, widespread inflammation, scarring, atrophy of glands in physiological breeding season, 0-10%, severe changes in endometrium
more fibrotic nests
endometrial swab in horse
need :clean uterine culture: for some stallions prior to breeding
culture and ctyology
when = late oestrus best because uterine flora decreaes with increase in estrogen
dog mammary tumour stage
use elston and ellis (Nottingham) method
–> tubule formation 1-3, nulclear pleomorphism 1-3 mitotic counts 1-3
total 3-5= grade 1, 6-7= grad 2 , 8-11 = grade 3 all is malignant
increased malignancy = decreased survival
cats mammy tumour staing
modified mnethods
sam grade of malignacy
grades of tumour
1= well-differentiated carcinoma
2= moderaltey differentieated
3= poorly differentiated carcinoma
TNM classification
T = primary tumour size
T1 = <3cm (d), <1cm (cats)
T2= 3-5cm 1-3cm
T3 = >5cm. >3cm
T4 = inflammation
N = lymph node invovlement
N0 = no mets (cyto/histo)
N1 = mets to ipsilateral LN
N2 = mets to contralateral LN
M= metastatic disease
M0 = no distant
M1 = distant mets
treatment of tumour
surgery
adjuvant jormone, chemo, radiatio, desmopressin, anti-cox2 treatemtn
not without surgery
anti-cox 2 inhibitors
- selective = firocoxib
- non-selectve meloxicam
in combo with chemo
for IMC = improved quality of lif
mammary tumour bitch
unspayed
influence of sex hromones/castration
<50% malignant
<25% mets to lungs
mammary tumour queen
lower prevalence than bithces
influence of sex hormones/castration
>90% malignant
mets to lung
vascularisation of mammary gland
T1+T2 = cranial superficial epigastric, lateral thoracic and intercostal arteries
A1 = cranial superficial epigastric with anastomses to caudal one
A2 + 1 = caudal superifical epigastric
veins follow artery pattern but small veins cross the midline = potential depostion of maligant cells in adjacetn gland
AT1 = cranial thoracic
T2 = caaudal thoracic
A1 cranial abdomina
A2 caudal abdomianl
I inguinal
lymphatic drainage
axillary LN = both thoracic
superficial inguinal = caudal abdo + inguinal gland
cranial abdo gland can be axillary +/or superifical inguinal
in neoplasic thoracic glands - superficial cervixal or ventral thoracic LN involved
both abdo glands drained by axillary, superficial inguinal + popliteal
inguinal drained big popliteal lymph lymph centre
risk factors for mama tumours
age
= risk increase wihth age (median 8y)
breed + genetic
= poodles, English sprigner, GSD, maltese, yorkiie
= no common genetic mtatuion found yet but BRCA 1+2 genes involve in English springer spangles= beagles = familial susceptibility
hormones and growth factors
= castration = best way to prevent
= befreo 1st heat = 0.5% risk
= before 2nd heat = 8%
= befoer 3rd heat = 26%
= preventative effect 0 after 4yr old
= number of pregnancies = no influencee
= more than 3 pseudolactation = incrase risk due to mechanic compression of acini and release of carcinogenic free radical
COX-2 expressin
- in jhumans
= cox-1 = in many tissues
= cox 2 - not innormal cells, induced by growht factors, inflam, oncogens, more frequent In malignancy
diet
= thin at 9-11 months old, decrease risk
obesity = decrease serum globulin - increased serum estrogen
adipose tissue = inreased estradiol production
high intake red meat
molecular pathogenesis in tumours
stem cells
= primary places of neoplastic transformation
estrogen
= growth factor production, direct genotoxic effect
progesterone
= synthesis of GH + it’s receptors(effects on mammary gland
mammary tumours in cats
rare
10-12 yr old
2x higher risk in siamese
high mortality and almost always malignant
OVH in 1st year = 90% preventive
mammary tumour signs
1 or more nodules in mammary gland
usually clinically health
severity of signs depemnds on extent and location of metastasis
-> lungs , live,r bone, brain, spleen, kidney, skin, eye
initial work up for tumour
age, age at OVH
history = duration of signs, repro cycles, lactation, progetsterone therapy
general condition and physical exam –> look at all mam glands in dorsal recumebcny and check LN
diagnosis of mamary tumour
blood and biochem
x-ray of thorax, CT will see 1mm
US
FNA + cytology = prediction of malignancy. 4 sampes per mass. good to differentiate from mastocytoa
check LN - biopsy/FNA for staging
treatment for mammary tumour
surgery = gold standard
exception = inoperable, higly metastic tumours or IMC
classification of tumour
epithelial
- simple adenoma/carcinoma -> invasive but good pronosis if completely removed
- epithelial and myoepithelial -> complex adeoma/carcinaoma > rare metasasis, prognosis semi good if compleelt removed
mesenhycma
- fibroadenoma/fibrosarcona, less than 5% of all mammary tumours
combo of epithelial and mesenchyma - very aggresive and poor prognosis
benefits of ET
faster genetic progress
offspring from old/injured animals
increased milk production in dairy herd
increased farm income through embryo sales (easier to transport and than live animals)
preserves superior genetics/endangered species
limitations of ET
decreased genetic diversity
expensive and time consuming
success rates less than AI
not all potential donors respond well
MOET
multiple ovulation embryo transfer
embryos flushed from donor and transferred to recipient
goal = obtain maximum number of genetically superior embryos in minimal amount of time
MOET select donor cow
based on produceer preference
has to be reproductively sound (no birthing difficulties, normal cycles etc)
disease free, appropriate BCS etc
MOET superovaulation of donro
9-11d after heat, give FSH, LH to induce ovulation
could give prostaglandins to cause estrus in 48-60h
85% of donors average 5 transferable embyros
purified FSH 2x1d for 4-5d
MOET insemination of donor
2-3 x at 12 h intervals 12h after onset of standing heat
semen put in body of uterus
MOET flushing embryos
7d after start of estrus
rectal US to assess superovulatory response (CLs) and give epidural
use a foley catheter, collection flask and flushing fluid
MOET selection and preparation of recipients
young dairy cows in good BC - repro sound
in heifer - 15m+, 350kg+ - cheap and better for synchro but possible calving problmes
syncorhinsed with PGF, gestated or Ovsynch
MOET transfer of embyros
load embryo in 0.25ml insemiahtion straw and low into ET gun
palpate recipient to see which ovary has CL and transfer to ipsilateral uterine horne
transfer within 8hr after flushing (can be frozen)
steps of MOET
select donor cow
superovualtion of donor cow
insemination of donor cow
flushing embyros
evaluate embyros
selection and preparation of recipient
transfer of embyros
APGAR
immediately for calves
within 1-3 mins for foals
2 = best
A= appearance
P=pulse
G=grimace
A=activity
R= respiration
scores
7-8 = vital
4-6 danger
0-3 avital
calves APGAR
activity
= check pupils and interdigital reflex
grimace
0=nothing
1= decreased
2= active
= check head movements under cold water
respiratory
0= nothing
1= arrhytmic
2= rhythmic
MM
0= pale/blue
1= cyanotic
2= pink
puppies APGAR
pulse
0= <180
1= 180-220
2= >220
respiration
0= none or <6
1= 6-15
2= >15
reflexes
0= no
2= present
MM
0= cyanotic
1= pale
2= pink
fetotomy
operations performed on fetus to decrease size by divison/removal of parts for vaginal delivery partial or total
when to do fetotomy
dead fetus
emphysematous fetus
fetus toobig/pelvis too narrow
fetus has abnormality
irreducible/incorrect 3Ps
fetus alive?
pinch toes/poke eyes -move away
put finger in mouth - sucke
check retail tone - should contract
kill fetus
use finger knife to cut vascular structures on neck or umbilicus
faster and less painful = head decapitation with fetotomy wire
after care, after fetotomy
remove every piece of fetus, check uterus for cuts/another calf, remove placenta, oxytocin, ATB locally or systemic if infected
advantage of fetotomy
little assistance needed
lower cost
less intense post op
avoids excessive maniupulation
disadvatntaghe of fetotomy
possible laceration of birth canal
exhaustion of dam
injury of vet
types of cut in fetotomy
transverse = section perpendicular to long axis of fetotome
oblique = section oblique to long axis of fetotome
longitudinal = section parallel to long axis of fetotome
method of fetotomy
subcutaneous/intrafetal
= remove enough parts of limbs to decrease size of fetus
lost of physical strength needed and time consuming
percutaneous/extrafetal method
danish (zagreb) method
anterior longitudinal presentaiton
head removal
oblique section of forelimb, next and part of thorac
section of pelvis or fetal trunk
bisection of pelvis
causes of dystocia
FETAL
oversized dfetus
congenital abnormality
abnormal orientation
MATERNAL
birth canal pathologies
felt membrane abnormalitis
placenta problems
why od pregnancy termination
unwanted mating
bithc too young/old
bitch health proglems
litter of no value
4 mechanism of preg termination
changing estrogen-progesteroen relation
- estrogen or glucocorticoids
inhibition of luteal function
- PGF or dopamine agonists
blocking progesterone synthesis by inhibiting steroidogenesis
- epostan
blocking progesteron activity on receptor leve
- aglepriston
inflammatory mamary carcinoma
rare, locally aggressive, fast growing, highly malignant,highhlt metastatic form of mammary tumour that affects humans and dogs
7.6% of mmamary tumours in dogs are IMC
IMC histologically
high grade carcinoma with dermal lymphatic invasion
anapaestic carcinoma
tubular, solid or mixed
high % of VEGF immunoreactive tumour cells meaning angiogenic and metastatic potential
forms of IMC
primary =
animals without history of previouss mamary nodules
secondary
= with history of previous mammary tumour
post surfical or non-post surgical
signs of IMC
edema, eryhtema, ucleration, warmth, firmness, pain
maybe lymphadema of limbs
uni or bilateral
can mimic severe mastitis and dermatitis
occurs in luteal phase of cycle due to progesteornr
metastasis of IMC
bladder
ovaries and uterus
rrrely to lung, liver bone and kdinsye
treatment of IMC
surgery not recommended
palliative care
adjuvant theray
chemo, cox-2inhibitors
v.poor prgonsosi - 60 days
pregnancy termination in cats
less common
oestrogen’s
PGF2a (dinoprost and cloprostenol)
dopamine agonist (cabergoline)
antiprogestin
surgical castration
gonadectomy
OVH
long term problems; obesity, rinary incontiencne, endocrine disorders, behaviour changes, neoplasia
non-surgical castraton
why= inconvenient estrus timing, pyometra management, contraception
least invasive - separate male and female
contraction havs to be: safe, cheap, efficient and easily applied
hormones for contraception
progestogens
androgens
GnRH agonist
GnRH antagonist
chemicals for contraceptiojn
zinc gluconadte
ca chloride
chlorhexiidne gddigluconate
hypertonic saline
progestogens
most frequently used method
in male animals = prevents sexually related behaviour eg spraying
contraceptive effect of progestogens
negative feedback effect on hypothalamus + pituitary
-> prevents stimulation of follicle growth and ovulation (continuous high conc suppress FSH+ LH production)
impede movement of sperm and eggs to site of fertilisation
interfere with implantation
side effects of progestogens
depend on type, dose, duration and age of animal
less if given in anestrus and small doseas
increase appetite, weight gain, lethargy, alopecia, adrenocortical suppression, acromegaly symptoms
uterine pathology - CEH, pyometra
mammary gland neoplasia
medroxyprogesterone acetate
long lasting injection
2mg/kg SC or 5mg PO for 21d max
return to estrus in 2-9 months
most adrogenic and immunosuppresivem
melengestrol acetate
temporary estrus suppression (can be used with GnRH agonist)
2.2mg/kg PO for 8 d early in proestrus
2-4w administration during anestrus
antiadrogenic, antiestrogenic, cortisol agent
contraception GnRH (agonist)
- suppression of GnRH suppresses reproductive steroid hormones therefore behaviour
worry over effect on non-target tissue
pros = good for male and female suppression estrus behaviour reversbiel
conc
= initial inducement of estrus and increase in temp (due to FSH and LH)
slow onset and variable duration injection or SC implant
deslorelin
implant for male (females and cats too)
4.7mg for 6m, 9.4mg for 12 m
dose dependent time for return to feritlity
nafarelin
18.5mg SC implant
-> 2ug/kg/day SC
last 8-11 mo after removal of implant im bitches and 3 year in cats
GnRH antagonsit
block GnRH receptors on pituitary cells without causing initial stimautlion of sexual behaviour
expensive - peptide on non-peptide molecules
generations: detirelix, acilin, degarelix, cetrorelix
pros = suppression for short time, suppresses estrus behaviour, reversible
non-peptides = cheaper and can be given PO, effect starts quicklyy
cons
= frequent applciation
reversible
no depo or long acting formaultions
first gen can cause histamine reaction in dogs
not in early pregnancy (LH)
2nd gen = luteal suppression + preg termination
3rd gen= preg termination and progesterone, decrease without side effects
melatonin
for cats
PO for 30-35d - implant better
short tem suppression -> 2-4 months, reversible, caution - initial induction of esters 12-18mg
prostaglandins
luteolytic and utertonic action
natural = dinoprosvt. synthetic = cloprostenol
dinoprosvt
= dose dependent side effects: hyper salivation, decreased HR, vomiting, that stops 1 h after admin, gradually increase dosage
cloprostenol
= more potent but decreased side effects, from 200-120d
dopamine agonist
effect D2 receptors -> decrease prolactin secretion -> decrease progesterone
decrease prolactin -> luteolytiss
bromocriptine = strong effect,ataxia and omiting
cabergoline = more efficient in smaller dose, milder side effects, movre peicfi cD2 receptors agonist and eodesn’t cross BBB as easy, efficient after 30d,
combined therapy
D2 agonists and PGF2a
-> 100% effective from day 25+, less side effects, don’t have to give everyday , cabergoline PO
aglespristone and PGF
misopristol = synthetic analogue of PGE, intravaginal - causes cervical dilation
combo with anglepirston = abortion in shorter duration (6d)
