branimira Flashcards

1
Q

maternal causes of dystocia

A

failure of expulsive forces (uterine or abdominal causes)

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2
Q

primary uterine inertia

A

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

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3
Q

secondary uterine inertia

A

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

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4
Q

abdominal causes of dysotica

A

Inability to strain
Causes : age, pain, debility, diaphragmatic rupture, tracheal / laryngeal damage

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5
Q

obstruction of birth canal

A

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

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6
Q

narrow pelvis

A

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

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7
Q

immature, juvenille pelvis

A

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

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8
Q

narrow vulva and vagina

A

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

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9
Q

narrow vertical canal

A
  • 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
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10
Q

stages of cervical canal (narrow cervical canal according to goetze)

A

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)

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11
Q

torsion of gravid uterus

A

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

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12
Q

endometritis in mares

A

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

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13
Q

physiological endometritis

A

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

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14
Q

PMIE

A

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

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15
Q

diagnosis of endometritis

A

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)

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16
Q

prevention of PMIE

A

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

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17
Q

chronic endometritis

A

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

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18
Q

pyometra as consequence of chronic endometirits

A

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

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19
Q

endometriosis

A

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

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20
Q

endometrial cysts

A

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

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21
Q

cause of infertility in cows

A

functional ovaires
displaying oestrus behaviour
narrow vagina
ovulation disorders
abortion
dystocia
detachment of placenta

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22
Q

freemartinism

A

most common non-inflammatory condition - 92% of heifers born to bull twins

results in infertility involving tubular reproductive tract

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23
Q

what are chimeras

A

individual animals that contain two cell types originating from separate zygotes

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24
Q

signs of freemartinsim

A

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

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25
Q

cause of freemartinism

A

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

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26
Q

diagnosis of freemartinism

A

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

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27
Q

prognosis of freemartins

A

most female cattle that are blood chimeras are often sterile freemartins

barren so use for fattening - not for mating

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28
Q

hermaphoriditism

A

mixing of sexual characteristics of both sexues in 1 individual

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29
Q

type of hermaphrodism

A

ambiglandular
testciular
ovarian

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30
Q

ambiglandular

A

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

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31
Q

testicular

A

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

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32
Q

ovarian

A

cause = enzymopathies in steroid conversio
chromosomal factors
heterosexual twins in cows
more rare than testicular

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33
Q

congenital repro problems cow

A

ovarian hypoplasia
congenital lesions on ovaries
abnormalities of uterine tubes
aplasia uteri
aplastic cervix
cervix duplex
uterus didelphys
vagina subsepta
hymen feminis persistens

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34
Q

ovarian hypoplasia

A

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

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35
Q

congenital leiosns on ovaries

A

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

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36
Q

cervix duplex

A

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

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37
Q

uterus didelphys

A

complete absence of fusion of 2 paramesonpehric canals

AI in ipsilateral horn-conception and AI possible

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38
Q

vagina subsepta

A

= 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

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39
Q

acquired repro problems co

A

ovaritis
ovarian neoplasia
lesions of uterine tube
mucometra
uterine tumours
uterine adhesions

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40
Q

urovagina - cow

A

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

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41
Q

ovarian cyst cow

A

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

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42
Q

how to help with anovulatory conditions in cattle

A

improve energy status during transition period

prevent disase

decrease frequency of suckling to 1-2 x1d in beef cows

GnRH agonist, prostaglandins or progestogens

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43
Q

differentials of ovarian cysts cattle

A

corpus hemorrhagicum
vaculoalted LC
non-ovarian cyst
abscess
tumour

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44
Q

types of ovarian cyst cattle

A

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

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45
Q

signs of ovarian cyst cattle

A

follicular = 80% anestrus, unequal esters or persistent anestrus, masculinisation
luteal = anestrus

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46
Q

risk factor of ovarian cyst cow

A

dystocia, RFM, NEB, obesity, increased temp, older, feeding oestrogen type components

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47
Q

cause of ovarian cyst cattle

A

neuroendocrine imbalance

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48
Q

therapy of COD cattle

A

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

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49
Q

prevention of ovarian cyst cow

A

decrease stress, treat infection, prophylactic GnRH 12-14d post birth

no effective treatment for multiple cysts so cull

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50
Q

absent or delayed ovulation

A

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

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51
Q

ovarian atrophy

A

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

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52
Q

bartholin gland cyst

A

= 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

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53
Q

penumovagina

A

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

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54
Q

RBC

A

= normally cyclic cow with no clinical abnormality which has failed to conceive after 3 successive insemination

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55
Q

pathologic conditions of RBC

A

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

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56
Q

treatment of RBC

A

intrauterine ATB 10-12h post insemination
- uterus can recover before embryo arrives in uterius at day 4-5
- give GnRH at time of insemination

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57
Q

cause and factors of RBC

A

cause = unclear but mulitfactorial
-> cow, bull, environment

factors: age, genetics, infection of repro tract, nutrition, embryo mortality

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58
Q

trauma in small rum

A

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

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59
Q

pseudopregnancy in goats

A

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

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60
Q

pregnancy toxaemia

A

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

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61
Q

pseudolactation

A

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

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62
Q

pathogenesis of pseudolactation

A

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)

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63
Q

signs of pseudolactation

A

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

64
Q

complications and dd of pseudolactation

A

rare - vomiting, anorexia, PUPD, tumours, mastitis, CEH

DD = rule out pregnancy, mastitis, tumour, pyometra

65
Q

diagnosis of peudolactation

A

signs and histroy
hormonal tests no due to specific physiology of sexual cycle of bitch

66
Q

treatment of pseudolactation

A

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

67
Q

what is feline mammary fibroepithelial hyperplasia

A

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

68
Q

pathogenesis of FEH

A

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

69
Q

pathomorphological characteristics of FEH

A

firm, well-circumscribed unencapsulated mass, solid and smooth

possible ulcerations and necrosis

micro=profieration of glandular, fibre - epithelial elements

70
Q

therapy and prognosis of FEH

A

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

71
Q

clinical findings of FEH

A

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

72
Q

complications of FEH

A

mastitis in lactating queens

ulceration due to overstretched skin

maybe hemorrhagic/purulent exudate

increase temp, lethargy, anorexia

LN involvement

73
Q

diagnosis of FEH

A

signs = spread of development
biopsy = FNA or excision - large amount of mitosis = false malignanyc

US - increased echogenicity
DD = neoplasia, FEH = bigger and softer

74
Q

congenital abnormalities in bitch

A

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

75
Q

transmissible venereal tumour dog

A

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

76
Q

cystic endometrial hyperplasia - bitch

A

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

77
Q

pyometra

A

progesterone mediated uterine disease occurring during diestrous

bacterial infection with opportunistic organisms from vagina secondary to CEH

most common organism = e.coli

78
Q

types of pyometra

A

open
= 4-8 weeks post estrus, vulvar discharge, less systemically ill

closed
= abdo distension, minimal discharge, more systemic signs

79
Q

signs of pyometra

A

fever
hypothermia
dehydration

80
Q

lab and diagnosis of pyometra

A

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

81
Q

therapy for pyometra

A

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

82
Q

split estrus dog

A

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

83
Q

vaginal prolapse dog

A

= 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

84
Q

pyometra queen

A

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

85
Q

endometrial biopsy mare

A

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

86
Q

categories of endometrial biopsy mare

A

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

87
Q

endometrial swab in horse

A

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

88
Q

dog mammary tumour stage

A

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

89
Q

cats mammy tumour staing

A

modified mnethods
sam grade of malignacy

90
Q

grades of tumour

A

1= well-differentiated carcinoma
2= moderaltey differentieated
3= poorly differentiated carcinoma

91
Q

TNM classification

A

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

92
Q

treatment of tumour

A

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

93
Q

mammary tumour bitch

A

unspayed
influence of sex hromones/castration
<50% malignant
<25% mets to lungs

94
Q

mammary tumour queen

A

lower prevalence than bithces
influence of sex hormones/castration
>90% malignant
mets to lung

95
Q

vascularisation of mammary gland

A

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

96
Q

lymphatic drainage

A

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

97
Q

risk factors for mama tumours

A

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

98
Q

molecular pathogenesis in tumours

A

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

99
Q

mammary tumours in cats

A

rare
10-12 yr old
2x higher risk in siamese
high mortality and almost always malignant
OVH in 1st year = 90% preventive

100
Q

mammary tumour signs

A

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

101
Q

initial work up for tumour

A

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

102
Q

diagnosis of mamary tumour

A

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

103
Q

treatment for mammary tumour

A

surgery = gold standard

exception = inoperable, higly metastic tumours or IMC

104
Q

classification of tumour

A

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

105
Q

benefits of ET

A

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

106
Q

limitations of ET

A

decreased genetic diversity
expensive and time consuming
success rates less than AI
not all potential donors respond well

107
Q

MOET

A

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

108
Q

MOET select donor cow

A

based on produceer preference
has to be reproductively sound (no birthing difficulties, normal cycles etc)
disease free, appropriate BCS etc

109
Q

MOET superovaulation of donro

A

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

110
Q

MOET insemination of donor

A

2-3 x at 12 h intervals 12h after onset of standing heat

semen put in body of uterus

111
Q

MOET flushing embryos

A

7d after start of estrus
rectal US to assess superovulatory response (CLs) and give epidural

use a foley catheter, collection flask and flushing fluid

112
Q

MOET selection and preparation of recipients

A

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

113
Q

MOET transfer of embyros

A

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)

114
Q

steps of MOET

A

select donor cow
superovualtion of donor cow
insemination of donor cow
flushing embyros
evaluate embyros
selection and preparation of recipient
transfer of embyros

115
Q

APGAR

A

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

116
Q

calves APGAR

A

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

117
Q

puppies APGAR

A

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

118
Q

fetotomy

A

operations performed on fetus to decrease size by divison/removal of parts for vaginal delivery partial or total

119
Q

when to do fetotomy

A

dead fetus
emphysematous fetus
fetus toobig/pelvis too narrow
fetus has abnormality
irreducible/incorrect 3Ps

120
Q

fetus alive?

A

pinch toes/poke eyes -move away
put finger in mouth - sucke
check retail tone - should contract

121
Q

kill fetus

A

use finger knife to cut vascular structures on neck or umbilicus
faster and less painful = head decapitation with fetotomy wire

122
Q

after care, after fetotomy

A

remove every piece of fetus, check uterus for cuts/another calf, remove placenta, oxytocin, ATB locally or systemic if infected

123
Q

advantage of fetotomy

A

little assistance needed
lower cost
less intense post op
avoids excessive maniupulation

124
Q

disadvatntaghe of fetotomy

A

possible laceration of birth canal
exhaustion of dam
injury of vet

125
Q

types of cut in fetotomy

A

transverse = section perpendicular to long axis of fetotome

oblique = section oblique to long axis of fetotome

longitudinal = section parallel to long axis of fetotome

126
Q

method of fetotomy

A

subcutaneous/intrafetal
= remove enough parts of limbs to decrease size of fetus
lost of physical strength needed and time consuming

percutaneous/extrafetal method

127
Q

danish (zagreb) method

A

anterior longitudinal presentaiton

head removal
oblique section of forelimb, next and part of thorac
section of pelvis or fetal trunk
bisection of pelvis

128
Q

causes of dystocia

A

FETAL
oversized dfetus
congenital abnormality
abnormal orientation

MATERNAL
birth canal pathologies
felt membrane abnormalitis
placenta problems

129
Q

why od pregnancy termination

A

unwanted mating
bithc too young/old
bitch health proglems
litter of no value

130
Q

4 mechanism of preg termination

A

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

131
Q

inflammatory mamary carcinoma

A

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

132
Q

IMC histologically

A

high grade carcinoma with dermal lymphatic invasion

anapaestic carcinoma

tubular, solid or mixed

high % of VEGF immunoreactive tumour cells meaning angiogenic and metastatic potential

133
Q

forms of IMC

A

primary =
animals without history of previouss mamary nodules

secondary
= with history of previous mammary tumour
post surfical or non-post surgical

134
Q

signs of IMC

A

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

135
Q

metastasis of IMC

A

bladder
ovaries and uterus
rrrely to lung, liver bone and kdinsye

136
Q

treatment of IMC

A

surgery not recommended

palliative care
adjuvant theray
chemo, cox-2inhibitors

v.poor prgonsosi - 60 days

137
Q

pregnancy termination in cats

A

less common
oestrogen’s
PGF2a (dinoprost and cloprostenol)
dopamine agonist (cabergoline)
antiprogestin

138
Q

surgical castration

A

gonadectomy
OVH
long term problems; obesity, rinary incontiencne, endocrine disorders, behaviour changes, neoplasia

139
Q

non-surgical castraton

A

why= inconvenient estrus timing, pyometra management, contraception

least invasive - separate male and female

contraction havs to be: safe, cheap, efficient and easily applied

140
Q

hormones for contraception

A

progestogens
androgens
GnRH agonist
GnRH antagonist

141
Q

chemicals for contraceptiojn

A

zinc gluconadte
ca chloride
chlorhexiidne gddigluconate
hypertonic saline

142
Q

progestogens

A

most frequently used method

in male animals = prevents sexually related behaviour eg spraying

143
Q

contraceptive effect of progestogens

A

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

144
Q

side effects of progestogens

A

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

145
Q

medroxyprogesterone acetate

A

long lasting injection
2mg/kg SC or 5mg PO for 21d max
return to estrus in 2-9 months
most adrogenic and immunosuppresivem

146
Q

melengestrol acetate

A

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

147
Q

contraception GnRH (agonist)

A
  • 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

148
Q

deslorelin

A

implant for male (females and cats too)
4.7mg for 6m, 9.4mg for 12 m
dose dependent time for return to feritlity

149
Q

nafarelin

A

18.5mg SC implant
-> 2ug/kg/day SC
last 8-11 mo after removal of implant im bitches and 3 year in cats

150
Q

GnRH antagonsit

A

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

151
Q

melatonin

A

for cats
PO for 30-35d - implant better
short tem suppression -> 2-4 months, reversible, caution - initial induction of esters 12-18mg

152
Q

prostaglandins

A

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

153
Q

dopamine agonist

A

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,

154
Q

combined therapy

A

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)

155
Q
A